General Health:
- Women:
Leading cause of death: **Cardiovascular
Highest cancer incidence: Breast Cancer
Highest cancer mortality: Lung Cancer
Pharmacology:
- Pindolol is classified as "partial beta agonist".
- Myasthenia gravis lady OD'ed on her Neostigmine tx and experienced severe muscle weakness. What was the mechanism of the drug causing the extra weakeness?
Normally MG auto-antibodies compete for binding to the nicotinic Ach receptor. MG treatment uses AchE's that keep Ach around so it can bind to what little unbound Ach receptors that are left. Neostigmine (AchE) overdose keeps too much Ach around which binds to the remaining receptors and effectively "desensitizes the receptors". Hence ans was "desensitization of nicotinic receptors".
- Guy on mountain taking Acetazolamide. Asked what was causing his orthostatic hypotension and ans was hypovolemia.
The carbonic anhydrase inhibitor (acetazolamide) helps in high altitude sickness because it causes acidosis, which counteracts the alkalosis caused by hyperventilation...HOWEVER it is also a diuretic, and so it would cause some hypovolemia in normotensive persons which can lead to orthostatic hypotension. The only other choice that can cause orthostatic hypotension is impaired sympathetic activity, but it is unrelated to acetazolamide.
Pathology:
- Lady with cerebral **AVM coronal cross section:
Other differentials for cystic spaces in the brain:
Piloastrocytoma (solid & cystic spaces)
Lacunar stroke (near internal capsule)
- Lady gaining weight despite dieting, hirsutism, purple striae, pituitary mass, etc--obviously has Cushing's Disease. Histological change in the adrenal cortex was Cortical HYPERPLASIA.
Physiology:
- ANP constricts efferent and dilates afferent. Remember it's trying to get rid of water because you are volume overloaded in CHF (so it's going to really increase your GFR: "brisk diuresis". If you increase flow to the nephron then you decrease the time you have to reabsorb Na+ so the macula densa decreases it's activity = decreased RENIN.
- Pt clearly had Nephrogenic Diabetes Insipidus (from the Lithium she was taking for her Bipolar Disorder & administration of Desmopressin didn't change anything)...had to pick values for tubular osmolarity, as comparing to serum osmolarity. Ans was:
Proximal Convoluted: Isotonic (**recall that reabsorption in the PCT is isotonic--the osmotic potential of the fluid leaving the proximal tubule is the same as that of the initial glomerular filtrate.)
Medullary Collecting Duct: Hypotonic
- Renal Artery Stenosis: Renin was HIGH in stenosed artery. (Dec RPF, slows down time macula densa sees solutes, increases renin release.)
Practice Q: If right renal artery is stenosed, then what will be the pattern of renin concentration in both the right and left renal veins?
- Right - HIGH renin
- Left - LOW renin
Right renal artery stenosis (hear bruit) causes DEC right renal perfusion pressure, INC renin secretion from the right kidney, and INC renin levels in the right renal vein. The INC renin secreted by the right kidney is added to the general circulation and leads to INC production of Angiotensin II, INC secretion of Aldosterone, and ultimately INC arterial pressure. The INC arterial pressure is “seen” by the normal left kidney, which responds appropriately by DEC its renin secretion.
Neuro:
- Lady presenting with CLASSIC "wet, wobbly, wacky" Normal Pressure Hydrocephalus with dilated ventricles (that does not result in increased subarachnoid space volume) but you picked Parkinson's instead because of the distractor term, "shuffling gait". DO NOT DO THIS AGAIN!!!!!!!!!!!!!
- Pt's left hand had 3 week hx of: numbness, loss of touch graphesthesia and loss of two-point discrimination. Location of lesion is in which of the following locations? Ans was B, post-central gyrus (somatosensory).
Biochemistry:
- Various names for Complex IV = Cytochrome Oxidase = Cyt a/a3. Inhibited by CO & cyanide. Mnemonic: "1 Q Before Complex Attacking Fires." FA 104.
- The impaired metabolic process in mitochondrial myopathies (MELAS: encephalopathy, lactic acidosis, stroke-like episodes) is due to failure in oxidative phosphorylation.
- Painter cleaning up paint thinner/varnish ends up with a toxicity that involved anion gap metabolic acidosis. Antidote inhibits which enzyme? Had to know it was methanol (formic acid) toxicity treated with Fomepizole which inhibits methanol (and ethanol) metabolism at the first step by blocking **Alcohol deydrogenase.
(Note: Classic vignette involves a painter painting a room in a submarine, experiencing dizziness--then exuberance--then irritability. The pt's sight can become severely restricted in one eye, pupils dilated, the optic disks pallid, and the retinal vein engorged. Gait can become uncoordinated and suffer from acidosis. Methanol is the the culprit, but remember that FORMALDEHYDE is what's doing the toxic damage. That's why you inhibit the enzyme leading to that intermediate. See reactions below. Mnemonic for methanol-induced blindness: "Drunk MEself blind..."
Ethanol vs. Methanol Metabolism
- Ethanol----(Alcohol Dehydrogenase)----->Aldehyde-----(Aldehyde dehydrogenase)------>Acetate
vs.
- Methanol----(Alcohol Dehydrogenase)--->Formaldehyde----(Aldehyde Dehydrogenase)---->Formic acid
- A receptor was defective that caused hypoglycemia to be corrected by epinephrine but NOT glucagon...Ans was glycogen receptor because all the other choices were common to both glucagon and epinephrine acting to initiate the G-protein sequence that ends up in activating glycogen phosphorylase and breaking down glycogen.
- The sequence (AATAAA) which is transcribed into (AAUAAA) is the signal required to start adenylation and formation of the poly A tail, and it is located downstream (3’) of the coding region...The function of the tail is to protect the mRNA from cleavage, so in its absence most of the mRNA would be broken down by the endonucleases in the nucleus. (Ie mutation = NO polyadenylation).
- Boy had a "missense mutation of the tyrosine kinase domain of the TrkA gene". If that was the only signaling defect in the pt, what was disrupted?
Only the downstream effects are affected. The receptor itself is okay, and still binds ligand. Only the kinase part is mutated. This prevents autophosphorylation and a failure to phosphorylate whatever kinase components that are found downstream in the cascade from this receptor.
Immunology:
- Question listing "Cancer Types" and their "Tumor Antigens", asking which would "produce the highest antibody titer", ie be the most immunogenic. Had to pick antigen that was NOT a self antigen, but a foreign one (ie HPV antigen as opposed to B-cell, Breast, Melanoma & Prostate Ca antigens).
Psychiatry:
- Withdrawal: 12 hours after birth baby sucks frantically and cries inconsolably. Overreacts to stimuli and has a marked startle response. Sx resolve over next 2-3 weeks. Mommy used which drug during pregnancy? (Concept is withdrawal--baby will present with sx opposite to drug he was "taking" in utero. Mom was taking an opiod--ans: heroin. Key terms for opiod withdrawal are "cold turkey" and "flu-like" symptoms.)
Note: Do NOT confuse with marijuana (hallucinogen) withdrawal, which presents with irritability, depression, insomnia, nausea, anorexia, peaks in 2 days and lasts 5-7 days. Cannibinoid receptors are Gi proteins. There are two, the one to remember is CB1 in the BRAIN.
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