NRTI's are associated with possible side effects of anemia, granulocytopenia, and myelosuppression.

The baby does not get any maternal IgM, IgA or IgE as they do not cross the placenta, so if IgM is found it may suggest the baby has encountered an infection in utero.

IgG is passed down to the baby as a means of passive immunity until the baby can form their own antibodies of different types. So if you see anything other than IgG (e.g. IgM) you know it must be d/t an infection.

Methanol is toxic by two mechanisms:

First, methanol can be fatal due to its CNS depressant properties in the same manner as ethanol poisoning.

Second, in a process of toxication, it is metabolized to formic acid via formaldehyde in a process initiated by the enzyme alcohol dehydrogenase in the liver. Methanol is converted to formaldehyde via alcohol dehydrogenase (ADH) and formaldehyde is converted to formic acid (formate) via aldehyde dehydrogenase (ALDH).

Formate is toxic because it inhibits mitochondrial cytochrome c oxidase, causing hypoxia at the cellular level, and metabolic acidosis, among a variety of other metabolic disturbances.

Foreign body inflammatory facial skin disorder characterized by firm, hyper-pigmented papules and pustules that are painful and pruritic. Located on cheeks, jawline, and neck.

Commonly occurs as a result of shaving (“razor bumps”), primarily affects African-American males.

Images: shorturl.at/fpwY1

This is an interesting one. I like to remember it this way: in people with narcolepsy, all the “right kinds” of sleep are happening at all the “wrong times” of day. During the day, when a power nap would typically throw you immediately into REM, this kid is only entering Stage 1 or 2 (lightest sleep = slightest noises jar him back to reality). At night, when he should peacefully drift into Stage 1, 2, and so on, he instead completely zonks out. Classic narcolepsy.

From UpToDate: “Narcolepsy can be conceptualized as a disorder of sleep-wake control in which elements of sleep intrude into wakefulness and elements of wakefulness intrude into sleep.”

In narcolepsy, there is a direct transition from wakefulness to REM sleep. Basically instead of going through the early stages and gradually falling into a deep sleep, you just suddenly go from being awake to being in a deep sleep.

Acyclovir, famciclovir, valacyclovir are guanosine analogs. They undergo conversion to acyclovir monophosphate via virus encoded thymidine-kinase. Ultimately, they inhibit viral DNA polymerase by chain termination.

Mutated viral thymidine kinase can cause resistance.

Earliest detectable secondary sexual characteristic is breast bud development in girls, testicular enlargement in boys.

Fronto-temporal dementia characterized by personality change is usually Picks

Frontotemporal dementia (formerly known as Pick disease): Early changes in personality and behavior (behavioral variant), or aphasia (primary progressive aphasia). May have associated movement disorders (eg, parkinsonism).

While this presents very similiarly to Hungtington's, you can differentiate it because in this stem it says "atrophy of the frontal lobes bilaterally" whereas Huntington's has atrophy of caudate and putamen with ex vacuo ventriculomegaly.

Little finger = ulnar nerve.

C8-T1 are the roots of the ulnar nerve, which is a branch of the medial cord. The ulnar nerve is not found in the carpal tunnel (the medial nerve is).

Ulnar n. damage can lead to loss of wrist flexion and adduction, flexion of medial fingers, abduction and adduction of fingers (interossei), actions of medial 2 lumbrical muscles. Loss of sensation over medial 1 1/2 fingers, including hypothenar eminence.

This has to do with intron splicing. Remember GTAG. This mutation induced an AG closer where it was supposed to be, so some of that intron just became an exon.

As described in the question stem, this mutation occurs within an intron (a gene segment which is transcribed [DNA->RNA] but not translated). RNA splicing enzyme(s) grab RNA and “loop it”; an intron is cut out and the exons on either side of the intron are adjoined, like this:

exon1—intron—exon2 => exon1—exon2

Typically, this splicing occurs at the very edges of the intron (what I denoted with the “—” character). But in our case, a mutation within the intron is causing RNA splicing enzyme to recognize a new site: the splicer cuts within the intron (instead of at the very edge, as it should). So, we get something that looks like this:

exon1—intr—exon2

That’s a totally different mRNA molecule, and it's going to make our β-globin protein look (and behave) awfully strange.

The mass described is in the posterior mediastinum (see images below). The thoracic duct is damaged “near the mass”, hence drainage of organs distal to that point will be affected. The images below should clarify.

Mediastinal relations.

Thoracic duct relations.

Thoracic duct relations.

The left upper extremity and breast are drained by the axillary lymph node. The kidney is drained by the thoracic duct. The heart has its own lymph system going on surrounding the heart.

headshot

https://slideplayer.com/slide/10842513/39/images/24/Drainage+territory+Drains+lymphatics+from+whole+of+the+body+except.jpg

No abnormalities, only some vomiting, looks well w/ no failure to thrive. Most likely immature LES.

Of all the options, psoas major is the only one that is really associated with the lumbar vertebrae.

Q. Lumborum involves the transverse process of L1 but Psoas Major originates from L1-L5

Definition of adjustment disorder:

Emotional symptoms (eg, anxiety, depression) that occur within 3 months of an identifiable psychosocial stressor (eg, divorce, illness) lasting < 6 months once the stressor has ended.

If symptoms persist > 6 months after stressor ends, it is GAD.

The pons has nerves 5-8, so the trigeminal would be affected here

Nowhere have I been able to find why the hell this is a thing.

As an edit: 108,001 people reported to have side effects when taking Hydrochlorothiazide. Among them, 25 people (0.02%) have Breast discharge

The tubes are catheters put in for urine to flow into a bag. So urine output is going to increase. The patient is also hyperkalemic. Aldosterone responds to hyperkalemia by increasing K+ excretion.

Hyperkalemia will stimulate aldosterone secretion even if renin is suppressed due to his hypertension. Although Na+ will be reabsorbed, this will be transient (should resolve once the potassium levels normalized) and since his urine output will most likely return to normal, his blood pressure should also normalize.

This patient has small cell carcinoma. This type of cancer is associated with paraneoplastic syndromes such as: Cushing Syndrome, SIADH, or antibodies against Ca2+ channels (Lambert-Eaton) or neurons. Amplification of myc oncogenes is also common.

SIADH (Syndrome of inappropriate antidiuretic hormone secretion) is characterized by:

• Excessive free water retention
• Euvolemic hyponatremia with continued urinary Na+ excretion
• Urine osmolality > serum osmolality

Body responds to water retention with aldosterone and ANP and BNP. That is what causes the increased urinary Na+ secretion Žwhich leads to normalization of extracellular fluid volume Žand the euvolemic hyponatremia.

Coarctation of the aorta leads to increased LV overload causing LV hypertrophy and a L axis deviation.

This is an example of Shingles. Herpes simplex and herpes zoster viruses cause abnormal cell division in epidermal cells, and this creates multinucleated giant cells.

A Tzank smear showing multinucleated giant cells is characteristic of Varicella Zoster Virus infections. (HSV will have similar findings).

Mycobacterium avium complex infections are a common opportunistic infection in patients with advanced AIDS (CD4 count <50).

This a CYP 450 inhibitor (SICKFACES.COM); its the O.

Add on to the other comment: SICKFACES.COM (when I Am drinking Grapefruit juice) is the mnemonic for remembering the CYP450 Inhibitors:

• S odium valproate
• I soniazid
• C imetidine
• K etoconazole
• F luconazole
• A cute alcohol abuse
• C hloramphenicol
• E rythromycin/clarithromycin
• S ulfonamides
• C iprofloxacin
• O meprazole

• M etronidazole

• A miodarone

• Grapefruit juice

Itraconazole requires the acidic environment of the stomach to be absorbed. Omeprazole inhibits the H+/K+ pump of the stomach, thereby decreasing the acidity of the stomach. So when the patient takes Omeprazole and Itraconazole together, Itraconazole won't be absorbed into the body. That's why it has no effect.

It's recommended to take medications at least 2 hours prior to taking an antacid.

Oxytocin uses IP3 signaling pathway.

GnRH, Oxytocin, ADH (V1-receptor), TRH, Histamine (H1-receptor), Angiotensin II, Gastrin.

FA mnemonic: "GOAT HAG"

So you know that 65% of the data will fall within 1SD of the mean. So if you subtract 100-65 you will get 35. Which means that about 16% will fall above and 16% will fall below 1 SD. They are asking for how many will fall above 1 SD. I'm sure there is a better way of doing this, but thats how I got it lol.

When you have a traveler who has intermittent abdominal symptoms and diarrhea, and who has traveled to the likes of northern Africa and such, Schistosomiasis needs to be on your radar. At least, that’s how I’ve incorporated this nugget into my mental space.

It also looked exactly like schistosome on the slide--it had the little spine. Entamoeba would have had a bunch of RBCs inside.

Trichomonas:

Clinical findings: thin, yellow-green, malodorous, frothy discharge and vaginal inflammation / itching.

Lab findings: pH >4.5 and motile trichomonads.

Lysine is used in elastin and collagen cross linking; it is cross linked by lysyl oxidase to make collagen fibers

Capitate and lunate are in the center of the palm. Capitate is not an option, so lunate is the answer.

Dislocation of lunate may cause acute carpal tunnel syndrome.

A radiographically visible air-fluid level suggests a pretty large lesion (hence, “cavitary”). That's not going to become normal tissue again. Six months following resolution of symptoms you can expect healing in the form of a scar; that is, fibrosis but only in a single spot.

This is the only choice that comes close to nicking the thoracic duct, specifically at its inlet, the left subclavian.

OK, so if I remember correctly this is the one that shows the inheritance pattern. mitochondrial is also passed by the mother; however, it can have variable expressivity and incomplete penetrance, which is why some members were not affected.

Missense mutations involve a nucleotide substitution resulting in changed amino acids. Sometimes the effects of missense mutations may be only apparent under certain environmental conditions; such missense mutations are called conditional mutations. Many missense mutations result in proteins that are still functional, at least to some degree.

Also, all the other answers would probably leave you with either a greatly altered or non-functional protein.

It affected the corticospinal tract in the crus cerebri on the L

The damage is in the L midbrain in the area affecting the corticospinal tract. Because it is in the midbrain, decussation in the pyramids (medulla) so it will show ipsilateral dysfunctional motor signs.

Photo of midbrain and important areas: shorturl.at/myHLR

Rhabdomyolysis can present looking like a kidney injury (it can lead to acute tubular necrosis as well). The electrolyte findings are just like renal failure (Inc. K+, inc. PO4-, dec. Ca)

To differentiate between rhabdomyolysis and kidney injury, you check the urine to see if there are any RBCs. In rhabdomyolysis there are no free RBCs in the urine.

With chronic vomiting, you lose electrolytes and a lot of acid. It triggers metabolic alkalosis which is why all the serum values are low (or on the lower end of the normal range) except for bicarbonate.

In metabolic alkalosis, potassium moves into the cells

The loss in volume through emesis triggers RAAS resulting in increased Aldosterone release and further potassium excretion

http://www.labpedia.net/test/116

Patient has a craniopharyngioma. Most common childhood supratentorial tumor. Derived from remnants of Rathke pouch (oral ectoderm). Calcification is common. Cholesterol crystals found in “motor oil”-like fluid within tumor.

A cystic suprasellar mass with calcifications and enhancement of the wall or solid portions in a child or adolescent is almost always a craniopharyngioma.

May be confused with pituitary adenoma (both cause bitemporal hemianopia).

Inguinal hernias are usually reducible, femoral hernias are not.

This is an indirect inguinal hernia. It enters internal inguinal ring lateral to inferior epigastric vessels and is superior to the inguinal ligament.

Caused by failure of processus vaginalis to close (can form hydrocele). May be noticed in infants or discovered in adulthood. Much more common in males.

Neoplasia is new tissue growth that is unregulated, irreversible, and monoclonal.

Clonality can be determined by glucose-6-phosphate dehydrogenase (G6PD) enzyme isoforms. G6PD is X-linked.

*For more information check out Ch. 3 Neoplasia in Pathoma

Prostatitis is characterized by dysuria, frequency, urgency, low back pain. Warm, tender, enlarged prostate.

Acute bacterial prostatitis—in older men most common bacterium is E. coli.

This patient has heart failure. Normal JVP is 6-8 mmHg.

Signs of heart failure are based on cardiac pump dysfunction, Žcongestion, and low perfusion.

Symptoms: include dyspnea, orthopnea, fatigue; signs include S3 heart sound, rales, jugular venous distention (JVD), and pitting edema.

The CI value contained 1, which means that its insignificant

Renovascular disease is the most common cause of 2° HTN in adults. Can be d/t ischemia from renal stenosis or microvascular disease. Can hear renal bruits lateral to umbilicus.

Main causes of renal artery stenosis:

• Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers.

• Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females.

Lab values based off:

1. Stenosis decreases blood flow to glomerulus.
2. Juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin I.
3. Angiotensin I is converted to angiotensin II (ATII) by angiotensin converting enzyme (ACE --in lungs)
4. ATII raises blood pressure by (1) contracting arteriolar smooth muscle, increasing total peripheral resistance and (2) promoting adrenal release of aldosterone, which increases reabsorption of sodium (where Na+ goes H2O will follow) in the distal convoluted tubule (expanding plasma volume). Can lead to hypokalemia (seen in the labs for this question)
5. Leads to HTN with increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary hypertension

Fanconi's is a generalized reabsorption defect in PCT causing increased excretion of amino acids, glucose, HCO3–, and PO43–, and all substances reabsorbed by the PCT.

Notice, the stem says "precorsors in the skin"

D3 (cholecalciferol) from exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants.

D2 (ergocalciferol) from ingestion of plants, fungi, yeasts.

Both converted to 25-OH D3 (storage form) in liver and to the active form 1,25-(OH)2 D3 (calcitriol) in kidney.

The two most important MI complications that occur within a 2-5 day span are papillary muscle rupture and interventricular septum ruture.

Papillary muscle rupture leads to severe mitral regurgitation, heard as a systolic murmur at the apex.

The strawberry hemangiomas tend to grow and then randomly involute.

Case of arteriolosclerosis.

Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')

• Consequence of malignant hypertension (>180/120 w/ acute end-organ damage)
• Results in reduced vessel caliber with end-organ ischemia
• May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure (ARF) with a characteristic 'flea-bitten' appearance

Short gastric a. branch from the splenic a.

Branches of the celiac trunk that constitute the blood supply to the stomach: common hepatic, splenic, and left gastric.

How to differentiate between Norovirus and Rotavirus here? Must be related to the the contagious nature of the illness?

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Most restriction enzymes bind palindromes.

So both 5'CCGG or 3'GGCC would have been acceptable in this scenario.

While the lifetime risk in the general population is just below 1%, it is 6.5% in first-degree relatives of patients and it rises to more than 40% in monozygotic twins of affected people. Analyzing classic studies of the genetics of schizophrenia done as early as in 1930s, Fischer concludes that a concordance rate for psychosis of about 50% in monozygotic twins seems to be a realistic estimate, which is significantly higher than that in dizygotic twins of about 10–19% (ncbi.nlm.nih.gov/pmc/articles/PMC4623659/#ref3)

Legionella is common causes of pneumonia superimposed on chronic obstructive pulmonary disease.

This is indirectly asking about peak bone density. That whole thing about weight-bearing exercises, eating right, yada yada, before and during that down-slope phase of life for bone density. All about reducing that 1% per year age-related bone density loss as best as we can. Level of activity is precisely like weight-bearing exercise. (Consider: no activity, bed-ridden -- say goodbye to your bones; highly active, runs every other day -- good amount of weight-bearing / stress to induce remodeling and maintain integrity of the bones.)

This is a hypoplasia of the pleuroperitoneal membrane. The guts herniate into the thorax, usually on the left side, and result in hypoplasia of the lungs (because they're horribly compressed).

Pelvic splanchnic nerves are part of the parasympathetic system.

Any answer with treponemes is used to syphilus only and is very specific. That only leaves cardiolipin, which is also elevated in SLE; this is why its sensitive but not specific in Syph.

Diagnosis of Syph: Visualized by immunofluorescence or dark-field microscopy; serology is important – two types of antibodies:

• Ab binds to cardiolipin: an antigen found in mammalian mitochondrial membranes and in treponemes; a cheap source of antigen is cow heart, which is used in screening tests; very sensitive in primary, except early, and secondary syphilis – titer may decline in tertiary and with treatment; but not specific – must confirm with FTA-ABS.

• Examples include Venereal Disease Research Lab (VDRL), Rapid plasma Reagin (RPR), Automated Reagin Test (ART), or Recombinant Antigen Test (ICE)

• Specific tests for treponemal antibody are more expensive; earliest antibodies bind to spirochetes: these tests are more specific and positive earlier; usually remain positive for life, but positive n patients with other treponemal diseases and may be positive in Mono, RF, Lupus, Leprosy, Lime, and Drug users.

• The most widely used is Fluorescent Treponemal Antibody- Absorption (FTA-ABS) or Treponema pallidum microhemagglutination (MHA-TP)

Encapsulated organisms run rampant in patients who have no spleen, whether physically or functionally. (Recall the wide-array of sequalae sickle cell patients experience thanks to their functional autosplenectomy.)

Dextromethorphan is an opium alkaloid derivative. Dextromethorphan is a drug of abuse. The main risks associated with dextromethorphan are ataxia, central nervous system (CNS) stimulation, dizziness, lethargy and psychotic behavior. Less frequently with large doses seizures and respiratory depression can occur. Nausea, vomiting, constipation and tachycardia may also occur. (toxnet.nlm.nih.gov)

Pt has polycythemia vera (myeloproliferative disorder) due to chronic hypoxia induced by COPD. Myeloid metaplasia is extra medullary hematopoiesis due to myelofibrosis. Hereditary hemochromatosis would have been proven by a prussian blue stain. Hypersplenism would have caused decreased RBCs, and myelodysplasic syndrome would have shown Auer rods or blasts.

This is reactive polycythemia vera, which is due to high altitude or lung disease. SaO2 is low, and EPO is increased.

Another way to approach the question is looking at the blood smear. It's pretty normal (no megakaryocytes, no increased number of platelets, no rods, nothing blue, etc). A blood smear from a COPD patient will be normal. Just an increased number of RBCs due to the increased EPO leading to increased Hgb.

ST will first decrease; however, after 20 min it will increase (elevate)

This man is showing sxs of an MI.

Initial phase of myocardial infarction leads to subendocardial necrosis involving < 50% of the myocardial thickness (subendocardial infarction); EKG shows ST-segment depression.

Continued or severe ischemia (>20 minutes) leads to transmural necrosis involving most of the myocardial wall (transmural infarction); EKG shows ST-segment elevation.

Is this the one with the poor kidney that was cut in half against its will and has a dilated distal ureter? If so, probably showing us transitional carcinoma with mild invasion into that distal ureter. Pathoma does a pretty awesome job of talking about GU cancers (and most cancers) ((and most medicine)) IMO.

It's transitional cell carcinoma, which smoking is a common risk factor for; it can involve the renal pelvis/calyces. The histo image shows the papillary nature of the tumor (however it can also be flat or nodular according to Pathoma).

Also known as urothelial carcinoma. Most common tumor of urinary tract system (can occur in renal calyces, renal pelvis, ureters, and bladder). Can be suggested by painless hematuria (no casts).

I have regarded crepitus as the rubbing of bone-on-bone. My study partner and I think this is a purely definitional question. Yes, crepitus could also be trapped air. Context, I guess.

Bronchophony= pneumonia Expiratory stridor= tracheobronchial obstruction (mass/foreign body) Inspiratory stridor = laryngeal obstruction Succussion splash= test for pyloric stenosis

When there is a fractured rib it will cause a trauma pnemothorax which can cause air to escape and become trapped under the skin leading to crepitus.

Here is a fantastic picture to understand

https://www.semanticscholar.org/paper/Pneumomediastinum-in-the-neonate.-Cagle/7b235daea2488612a1917009afc849afc3e262e7/figure/4

Cat scratch disease (Bartonella infection in immunocompetent hosts) causes lymphadenitis (especially in the axillary region) characterized by sarcoid-like non-caseating granulomas filled with neutrophils.

In eukaryotic cells, two major pathways—the ubiquitin-proteasome pathway and lysosomal proteolysis—mediate protein degradation.

The major pathway of selective protein degradation in eukaryotic cells uses ubiquitin as a marker that targets cytosolic and nuclear proteins for rapid proteolysis.

The other major pathway of protein degradation in eukaryotic cells involves the uptake of proteins by lysosomes and digestion by proteases.

Patient has chronic diarrhea leading to metabolic acidosis. Respiratory compensation will lead to decreased CO2 (respiratory alkalosis via hyperventilation).

I think the point of the question is to recognize that this is a mitochondrial disease (mother and maternal grandmother were affected). Produces wide range of effects, but muscle weakness and some neurologic deficits stood out to me. Also this: https://ghr.nlm.nih.gov/gene/MT-TL1#conditions

This is a presentation of mitochondrial myopathy. They often present with myopathy, lactic acidosis, and CNS disease. 2° to failure in oxidative phosphorylation. Muscle biopsy often shows “ragged red fibers”.

There is variable expression in a population or even within a family due to heteroplasmy in mitochondrial inheritance.

It's a mitochondrial disease. - present in successive generations, always with maternal transmission - damage to high-energy tissues - CSF lactic acidosis (due to increased anaerobic metabolism due to impaired oxidative phosphorylation)

Decreased total, normal free (unbound) = Thyroid hormone-binding globulin deficiency

Annular pancreas is the only answer that accounts for the bile in the vomit; of the choices, it is the only obstruction distal to where bile enters the GI tract.

Also, Meckels would have describe hematochezia or failure to pass meconium

Most important cause of viral myocarditis is Coxsackie (picornavirus).

He's not eating enough.

One of cortisol's functions is to increase gluconeogenesis, lipolysis, and proteolysis.

This is a conditional called craniocleidodysplasia. The kid on Stranger Things with the lisp has the disorder. No collar bones, too many teeth, frontal bossing => craniocleidodysplasia. CBFA1 is a gene highly implicated in osteoblast function.

A big thing here too is noticing that the ALP is decreased. Osteoblast activity is measured by bone ALP. I think that was the main focus here and not that you necessarily need to know the CBFA1 gene mutation.

They tell you that the kid has no clavicle. This means the defect is in membranous ossification, NOT endochondral, so the pathology is NOT going to involve the chondro-whatever cells. decreased ALK is consistent with osteoblast defect.

Pt has diabetes inspidus.

If urine concentrates with administration of ADH analog, the kidneys are responsive and the problem is with ADH production in the hypothalamus or release in the post. pituitary.

WHY she has a huge ass liver too? I don't understand how you can choose big spleen over big liver or visa versa

Liver looks pretty normal-sized to me. Pic here for comparison

I thought the liver looked huge af too lol which made me requisition the whole radiograph

Looked like hepatosplenomegaly, but I went with liver b/c the edema could be due to liver dysfunction.

Benign tumors are usually well-differentiated and well-demarcated, with low mitotic activity, no metastases, and no necrosis.

Malignant tumors (cancers) may show poor differentiation, erratic growth, local invasion, metastasis, and apoptosis. High mitotic activity.

Fat tumors:

• Lipoma: benign, low mitotic activity
• Liposarcoma: malignant, increased mitotic activity

Lipomas/Liposarcomas are the commonest soft-tissue tumors in adults. The high mitotic index & infiltrative nature indicate that the mass is malignant.

Defective homologous recombination is seen in breast/ovarian cancers with the BRCA1 gene mutation.

Ok, so you can reason this by drawing out REIT (sorry I can't draw it here). Anywho, you know its a restrictive disorder and will have a decreased RV, so automatically you know that RV is a component of FRC (FRC= RV+ERV). Thus, FRC should also be decreased. You also know that restrictive diseases are characterized by a steady decrease in FEV1/FVC since both components are decreasing. This leaves you with VC decreasing since FVC= forced vital capacity.

Mycoplasma pneumoniae cold agglutinins, no response to amoxicillin.

FA 2017: Classic cause of atypical “walking” pneumonia (insidious onset, headache, nonproductive cough, patchy or diffuse interstitial infiltrate). X-ray looks worse than patient. High titer of cold agglutinins (IgM), which can agglutinate or lyse RBCs. Grown on Eaton agar. Treatment: macrolides, doxycycline, or fluoroquinolone (penicillin ineffective since Mycoplasma have no cell wall). ABC = Africa, Blindness, Chronic infection. D–K = everything else. Neonatal disease can be acquired during passage through infected birth canal. No cell wall. Not seen on Gram stain. Pleomorphic A. Bacterial membrane contains sterols for stability. Mycoplasmal pneumonia is more common in patients < 30 years old. Frequent outbreaks in military recruits and prisons. Mycoplasma gets cold without a coat (cell wall).

Squamous cell carcinoma characteristics: cavitation, hypercalcemia, associated with smoking.

Small cell may actually produce antibodies against presynaptic Ca channels.

This is mullerian agenesis. Normal ovaries but absent uterus.

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Down Syndrome Labs:

• inc. nuchal translucency
• inc. hCG
• inc. inhibin
• decreased AFP
• decreased PAPPA

Absolute risk: the difference in risk (not the proportion) attributable to the intervention as compared to a control.

(.12) - (.04) = .08

ARR = 8%

I chose this solely because it was so damn specific

You have a 25% chance of inheriting the same HLA markers as your siblings.

Most of the pts values were normal. Drinking wasn't outrageous, LDL was mild, BMI has fine. He did have HTN though. The biggest risk factors are the fact that he had suffered an MI and started suffering severe depression (weight loss/anxiety). Thus, he is more at risk for suicide.

Beta blockers as antiarrhythmics suppress abnormal pacemakers by decreasing the slope of phase 4 --> prolonging phase 4.

p + q = 1 p^2 + 2pq + q^2 = 1 if q^2 = 1/1600 = 0.00063 then q = sqrt(q^2) = 0.025 solve for p to get p = 1 - r = 1 - 0.025 = 0.975 the heterozygous carriers = 2pq = 1 - p^2 = 1 - 0.95 = 0.5 q^2 can be dropped b/c it's much smaller than p^2. The deletion is responsible for 80% of the mutations. 0.8 x 0.5 = 0.04 = 4/100 = 1/25

There might be an easier way to do this, but it worked for me.

Allopurinol inhibits xanthine oxidase. It is used for chronic gout as well as prevention of tumor-lysis associated urate nephropathy.

Patient has medullary carcinoma. Malignant proliferation of parafollicular "C" cells that produce calcitonin and have sheets of cells in an amyloid stroma.

FA 2017: Infects B cells through CD21. Atypical lymphocytes on peripheral blood smear G —not infected B cells but reactive cytotoxic T cells. ⊕ Monospot test—heterophile antibodies detected by agglutination of sheep or horse RBCs. Use of amoxicillin in mononucleosis can cause characteristic maculopapular rash.

Methotrexate would be a drug of choice for psoriasis refractory to topical creams and light therapy; inhibits dihydrofolate reductase in order to decrease skin cell proliferation and reduce inflammatory response.

Leukotriene B4 is a potent chemotactic molecule for neutrophils. Selective loss of this would have no effect on platelets, mast cells, or endothelium - these are more responsive to changes in TXA2, complement/arachidonic acid, and PGI2, respectively.

Atrophy is decrease in tissue mass due to decrease in size (increased cytoskeleton degradation via ubiquitin-proteasome pathway and autophagy;  decreased protein synthesis) and/or number of cells (apoptosis). Causes include disuse, denervation, loss of blood supply, loss of hormonal stimulation, poor nutrition.

If prostate cancer spreads to other parts of the body, it nearly always goes to the bones first (cancer.org/cancer/prostate-cancer/treating/treating-pain.html)

Auto dom disease are usually heterozygous (or so they want us to assume)

Acute interstitial renal inflammation. Pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity (eg, diuretics, NSAIDs, penicillin derivatives, proton pump inhibitors, rifampin, quinolones, sulfonamides).

You are aiming to increase power and you can do so by increasing sample size (reduce B error).

Substance P (SP) is an undecapeptide present in the CNS and the peripheral nervous system. A compound thought to be involved in the synaptic transmission of pain and other nerve impulses.

Familial adenomatous polyposis is an autosomal dominant mutation. Thousands of polyps arise starting after puberty; pancolonic; always involves rectum. Prophylactic colectomy or else 100% progress to CRC.

Autosomal dominant diseases have, on average, 50% chance of being passed down to offspring.

Sensitivity tests are used for screening. Specificity tests are used for confirmation after positive screenings.

Sensitivity tests are used for seeing how many people truly have the disease. Specificity tests are for those who do not have the disease.

A highly sensitive test, when negative, rules OUT disease. A highly specific test, when positive, rules IN disease. So, a test with with low sensitivity cannot rule out a disease. A test with low specificity can't rule in disease.

The doctor and patient want to screen for colon cancer and rule it out. The doctor would want a test with high sensitivity to be able to do that. He knows that testing her stool for blood will not rule out the possibility of colon CA.

GnRH agonists like Leuprolide are effective for patients with breast CA because if given in a continuous fashion, they downregulate the GnRH receptor in the pituitary and ultimately decrease FSH and LH.

If you want to clear a drug, it is probably best that it not be bound to proteins (so that it gets filtered) and it has a low volume of distribution (so it isn't in the deep, hard to reach tissues).

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I was wondering if it was to allow for partial CNS penetration since the drug is supposedly supposed to have CNS effect

In order for a drug to be cleared by the kidney, it must first be filtered in the glomeruli. Drugs with a high VD have more of the drug in the tissue that are not available to filtered by the kidney. Drugs with high protein binding won't be filtered either. So you want a drug with low Vd and low binding if you want it cleared via the kidneys and urine.

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Can somebody please explain why the pKa has to be 6 instead of 10?

Patient has congenital hypothyroidism (cretinism). Findings: pot belly, pale, puffy-faced, umbilical hernia, macroglossia, hypotonia, poor brain development (MC cause of treatable mental retardation), large anterior fontanelles.

Most common cause of gastric outlet obstruction in infants. Palpable olive-shaped mass in epigastric region, visible peristaltic waves, and nonbilious projectile vomiting at ∼2–6 weeks old.

Ultrasound shows thickened and lengthened pylorus. Treatment is surgical incision (pyloromyotomy).

FA2019 page 47: I-cell disease (inclusion cell disease/mucolipidosis type II)—inherited lysosomal storage disorder; defect in N-acetylglucosaminyl-1-phosphotransferase → failure of the Golgi to phosphorylate mannose residues (forming mannose-6-phosphate) on glycoproteins → proteins are secreted extracellularly rather than delivered to lysosomes. Results in coarse facial features, gingival hyperplasia, clouded corneas, restricted joint movements, claw hand deformities, kyphoscoliosis, and high plasma levels of lysosomal enzymes. Often fatal in childhood.

Statins can have a side effect of rhabdomyolysis.

Heparin-induced thrombocytopenia (HIT) is the development of IgG antibodies against heparin bound platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets Ž thrombosis and thrombocytopenia. Highest risk with unfractionated heparin.

Septic shock is a type of distributive shock which is marked by massive vasodilation (d/t inflammatory response) causing decreased SVR, decreased preload / PCWP, and increased CO.

The right and left ventricle are drained by separate parts of the foramen of monro. (Left side is drained by left monro, right side by right monro). An obstruction of the right foramen of monro will enlarge the right ventricle.

Beta-Tubulin is a subunit of tubulin. Tubulin is one of several members of a small family of globular proteins. It is the major constituent of microtubules. There are two of most common members of the tubulin family: alpha-tubulin and beta-tubulin, and together their dimers form microtubules. (origene.com)

Administration of Penicillin for Syphilis may lead to the Jarisch-Herxheimer reaction hours after treatment. Occurs due to lysis of spirochetes (so it can occur with Borrelia and Leptospirosis as well). The reaction is characterized by fever and chills.

The classical explanation of the Herxheimer reaction is that treatment results in the sudden death and destruction of large numbers of treponemes, with the liberation of protein products and toxins.

CMV is associated with infecting organ transplant patients. CMV is transmitted via sexual contact, organ transplant, or vertically via placenta. Reactivation of CMV occurs in the immunosuppressed.

Organ transplant patients are at an increased risk of CMV pneumonia.

I think Shigella is the most appropriate, as it is actually regarded as highly inflammatory. Yes, E. coli can be of the EHEC/STEC variety, but E. coli could also be of the ETEC variety or whatever other strains it has. Ergo, E. coli may be plausible, but it is not the 'most likely.' Bleh to these kinds of questions.

Apart from the line in FA referencing PMN infiltrate in Shigella, there is no way to differentiate here between it and E. Coli. Cheap shot.

Methylene-blue stained fecal smear reveled numerous neutrophils (but not any organisms). Shigella is colorless when stained with methylene blue; E coli stains blue with methylene blue because it ferments lactose.

Shigella causes an inflammatory diarrhea; it produces a toxin and can invade tissue directly. In addition, it is resistant to acid, so it has a characteristically low infective dose (~10 organisms), which facilitates its fecal-oral (person-to-person) spread especially in settings where hygiene may be compromised, such as in daycare or institutional housing. It can be differentiated from E. Coli (EHEC) because E Coli doesn't have as much person-to-person spread and only causes GI damage by the shiga-like toxin, not direct invasion. Therefore, EHEC wouldn't facilitate as strong of a neutrophilic response.

Clinical use of K-sparing diuretics:

• Hyperaldosteronism
• K+ depletion
• HF
• hepatic ascites (spironolactone)
• nephrogenic DI (amiloride)
• antiandrogen

In psychogenic polydipsia, serum sodium is low, and after water deprivation test, urine osmolality is increased. Urine osmolality does not increase with vasopressin injection

In nephrogenic diabetes insipidus, serum sodium is high and there is no change/mild increase in urine osmolality after water deprivation

Isotretinoin is used to treat severe cystic acne. It is a teratogen. Can cause multiple severe birth defects. Contraception is mandatory. RXR is a retinoid X receptor.

IsoTERATinoin

The only time you transfuse a Jehovah's Witness patient is when the patient is a minor (<18 years old).

Other kidney Hypertrophies due to increased stress --> not hyperplasia bc not cancerous

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4946499/

Cilostazol is a phosphodiesterase inhibitor; leads to increased cAMP which inhibits platelet degranulation/activation while also causing vasodilation. All of the other options work on either vasculature or platelets but not both.

LV stopped working, pressure backed up into pulm circuit. Pulm circuit roughly is made of 3 "parts" - the capillaries, interstitial space, and the alveoli.

In cardiogenic shock, the extra blood increases capillary hydrostatic pressure, driving fluid into the interstitial space. Compared to the alveoli, the interstitial space now has more fluid (thus more interstitial hydrostatic pressure and less oncotic pressure due to ratio of fluid to protein), and as a result of this unbalancing of forces, fluid moves into the alveoli --> pulmonary edema.

Large swollen rectal veins --> patient has external hemorrhoids. Swollen and inflamed veins in the rectum and anus that cause discomfort and bleeding. The most common cause of external hemorrhoids is repeated straining while having a bowel movement.

By age 75, the thymus is little more than fatty tissue. Fortunately, the thymus produces all of your T cells by the time you reach puberty. They are long-lived and that's why you can lose your thymus without impairment of your immune system.

Not sure about this, but it seems to me that this is referring to "pseudocholinesterase inhibitor deficiency. It's an enzyme defect that is triggered by NMJ blockers - succinylcholine or curare's.

https://en.wikipedia.org/wiki/Pseudocholinesterase_deficiency

Amiodarone, a class III antiarrhythmic drug, has multiple effects on myocardial depolarization and repolarization that make it an extremely effective antiarrhythmic drug. However, amiodarone is associated with a number of side effects, including thyroid dysfunction (both hypo- and hyperthyroidism), which is due to amiodarone's high iodine content and its direct toxic effect on the thyroid. (uptodate.com)

Actinic purpura results from extravasation of blood into the dermis. This phenomenon is due to the skin atrophy and the fragility of the blood vessels in elderly individuals, which is exacerbated by chronic sun exposure. Actinic purpura lesions are located on sun-exposed areas, like the arms, face, and neck.

Skin atrophy in dermatoporosis is due to an alteration of collagen, similar to that which is seen in osteoporosis. This pronounced skin atrophy caused by the photo-aging makes the dermal vascular network very sensitive to the slightest trauma or shearing force.

Full article: https://www.ncbi.nlm.nih.gov/books/NBK448130/

They are talking about Baclofen, a GABA-B agonist known to treat muscle spasticity

This patient likely has some form of upper motor neuron lesion or disease - UMN lesions are characterized by weakness, increased deep tendon reflexes, and spastic paresis. Baclofen is a GABA-B agonist specific to the spinal cord, used ot treat muscle spasticity, dystonia, and MS. GABA-B is a G-protein coupled receptor coupled to Gi, so agonism of this receptor causes hyperpolarization of the neurons and decreased release of excitatory glutamate.

B-HCG and LH,FSH,TSH share same alpha subunit, so HCG can activate those receptors if its in high enough quantity. Activating LH receptor will lead to more Testosterone from the Leydig cells. More testosterone can lead to more estrogen formation via aromatase.

Sounds like a hypertrophic scar. "Hypertrophic scars contain primarily type III collagen oriented parallel to the epidermal surface with abundant nodules containing myofibroblasts, large extracellular collagen filaments and plentiful acidic mucopolysaccharides." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022978/

A fractured cribriform plate (anterior skull trauma) can result in leaking of cerebrospinal fluid into the nose and loss of sense of smell. Smell plays a large role in the perception of taste. So, in practice, a patient may complain of loss of taste rather than of smell.

Alcohol withdrawal leads to a sympathetic-hyperactivity-like syndrome with tremors, HTN, insomnia, GI upset, diaphoresis, and mild agitation 3-36 hours after the last drink. There is a similar, but usually slightly later, overlap of withdrawal seizures 6-48 hours after the last drink.

Single enhancing lesion points more towards lymphoma than toxo. Toxo is usually multi-ring enhancing lesions.

This is a primary central nervous system lymphoma. Most commonly associated with HIV/AIDS; pathogenesis involves EBV infection.

Considered an AIDS-defining illness. Variable presentation: confusion, memory loss, seizures. Mass lesion(s) (may be ring-enhancing in immunocompromised patient) on MRI, needs to be distinguished from toxoplasmosis via CSF analysis or other lab tests. Toxo usually has multiple ring enhancing lesions.

Hypertension can lead to aneurysms like in this patient. Not syphilis because not thoracic aorta.

FA 2017: 3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilatation of aorta and valve ring. May see calcification of aortic root, ascending aortic arch, and thoracic aorta. Leads to “tree bark” appearance of aorta. Can result in aneurysm of ascending aorta or aortic arch, aortic insufficiency.

She has a vitamin C deficiency. Scurvy features swollen gums, easy bruising, petechiae, perifollicular and subperiosteal hemorrhages.

Hydrocodone/Methadone can lead to dependence--you avoid in long term use. NSAIDs you also avoid due to partial ineffectiveness in neuropathic pain as well as ulcer risk. TCA's are known to treat neuropathic pain very well (i.e. diabetes, ART therapy)

Hypercarbia causes cerebral vasodilation. If you have ever seen an intra- or acute post-op neurosurgical patient, or really any patient about to herniate, you can remember this because they will be hyperventilated to pCO2 around 25-30 to decrease ICP via cerebral vasoconstriction; in this case, we have the opposite. The curve of pCO2 vs cerebral blood flow is quite steep in the physiologic range meaning small changes in ventilation make a significant difference in CBF.

The more general principle: endothelia vasodilate in the presence of high CO2; you gotta get rid of that acid somehow! Can’t let it accumulate, as lower pH within a “micro-environment” affects structure/efficiency of enzymes, proteins, etc. The more acidic a local environment, the more you expect nearby vasculature to dilate (as a means of increasing flow rate, thereby ferrying off accumulate acid).

The anesthesiologist can exploit this mechanism. By hyperventilating (blowing off CO2), the brain vasculature senses a low CO2 / “hunky-dory state,” which requires no vasodilation. In other words, the vasculature does not need to continue the ATP-consuming practice of synthesizing Nitric Oxide (NO).

Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP.

He wants to increase ICP (cerebral vasodilation) which he can do by decreasing the respiratory rate (hypoventilation).

https://drawittoknowit.com/pop-quizzes/anatomy-physiology/at-a-high-flow-rate-how-does-saliva-compare-to-plasma

As a rule of thumb, if you give someone an ACE inhibitor and they get a problem, they had renal artery stenosis (usually bilaterally, or so we were taught at our med school). Probably has to do with decreased GFR thanks to decreased Angiotensin II–selective vasoconstriction of the efferent arteriole => decreased sodium delivery to macula densa => increased renin release.

Also, you shouldn't be seeing end-organ damage or increased renin / kidney response with a previously healthy patient that just developed essential HTN. The body doesn't want to increase renin when it has HTN. However, if you have stenosis, the kidneys freak out because they're not getting enough flow and think the whole body isn't either, so they activate the RAAS system. When you give them an ACE-I, the renin is still being produced by the kidney, it just isn't being converted to angiotensin-II.

To eliminate other choices:

• He has increased renin activity so you can eliminate primary aldosteronism. That has inc. aldosterone, dec. renin.
• No signs or sxs of Cushing's so that's eliminated.
• 11-B-hydroxylase deficiency would sxs with the genitalia. You'd have dec. renin activity (aldosterone-like effects still present).
• Essential HTN: explained above

Zollinger-Ellison syndrome: Gastrin-secreting tumor (gastrinoma) of pancreas or duodenum.

resonant sound is normal. hyperresonant with overexpansion. tactile fremitus is increased /c solid mass or fluid, and decreased with air/fluid level or overexpansion. prolonged expiratory phase -> obstructive conditions.

This sounds like Fanconi syndrome. The proximal tubular epithelial cells have a hard time reabsorbing filtrate, so you'll see a loss of phosphate, amino acids, bicarbonate, and glucose.

This patient is experiencing hypersensitivity pneumonitis from the parakeets. I was thinking M. Avium when I selected parakeets -- I think my logic was flawed given the specifics of the patient's story.

I also was thinking M. avium here, but hypersensitivity pneumonitis seems to fit with the reticulogranular changes.

Hypersensitivity pneumonitis—mixed type III/IV hypersensitivity reaction to environmental antigen. Causes dyspnea, cough, chest tightness, headache. Often seen in farmers and those exposed to birds. Reversible in early stages if stimulus is avoided.

It's a type of restrictive lung disease.

Page 2 has a great picture

https://www.jacionline.org/article/S0091-6749(18)31602-6/pdf

Cyclosporine is a calcineurin inhibitor, which aims to decrease IL-2

As a side note, the phosphatase would have activated calcineurin https://www.ecosia.org/images?q=calcineurin+phosphatase#id=2E5AEA65CD7AADC5FADD1C144FFFAD3B7068FDAA

The adductor pollicis muscle is innervated by the ulnar nerve, giving this guy a difficult time holding a sheet of paper.

Most of intrinsic muscles of the hand are innervated by ulnar nerve - chronic compression at the hook of hamate could lead to nerve ischemia

Propanolol is a non-selective Beta blocker. So your HR will decrease (B1), which will cause a compensatory increase in TPR.

An adverse effect of doxycycline is photosensitivity.

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Anytime you have a person who bumps their head, gets back up, and then has severe issues or dies like 6 hours later -- you have yourself an epidural hematoma from laceration to the middle MENINGEAL artery. (Goljan really emphasizes that you don't screw up and select middle cerebral.) You know it has to be an arterial laceration since the dura is tightly adhered to the skull's inner surface. Goljan referred to his experience with it as needing pliers to remove the dura from the skull; graphic, but it drives the point home. Tenting seen on CT is because the epidural hematoma gets stuck between the suture lines. When it manages to break past one of the suture lines, it is my understanding that then is when you get severe sequelae, like death or whatever.

Iron overdose is a cause of a high anion gap metabolic acidosis.

Glucagonoma: Tumor of pancreatic α cells Žcausing an overproduction of glucagon.

Presents with 5D’s:

• Dermatitis(necrolytic migratory erythema)
• Diabetes (hyperglycemia)
• DVT
• Declining weight
• Depression

The first sentence acknowledges the patient's emotions, which is always good. The second sentence is good because it begins the interview with an open-ended question.

Answer is Astrocyte. Patient has glioblastoma multiforme. Although meningiomas may occur at convexities, meningiomas are benign and often asymptomatic. They may cause h/a seizures, but would be unlikely to cause death w/in 6m of onset of h/a. The size of tumor and course of illness is consistent with the course of GBM

You have negative Nitrogen balance in starvation (lack of protein) and positive Nitrogen in muscle building states (i.e. children/athletes)

Thought this would be something regarding "bariatric surgery," but nope, just "no starchy foods, because you're pre-diabetic."

I had put "starches" b/c pts that undergo bariatric surgery are only supposed to eat complex carbs (fruits/vegetables) and avoid simple carbs (i.e. breakfast cereal/baked goods)

Obstructive uropathy causes a postrenal azotemia --> when prolonged, tubular damage ensues. This leads to an acute tubular necrosis, characterized by necrotic plugs in the tubular system as seen in the image

Pt. has Familial dyslipidemias. Type I—Hyperchylomicronemia.

There are certain situations in which you don't need to notify parents about anything when treating a child--STIs are one of them. The reason being that untreated STIs will cause more spread as well as can lead to PID