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23 Cards in this Set
- Front
- Back
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Kartagener’s syndrome
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Immotile clia due to dynein arm defect
Only causes male infertility - not female. Ovum move down fallopian tube by peristaltic 蠕动 contractions - stimulated by estrogen, inhibited by progesterone. Ciliary motility do not appear to be necessary for female fertility. I read or heard that the female can't get pregnant due to her decreased ciliary action to sweet the egg. |
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Chorion vs. Amnion
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Hypokalemia and digoxin
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hyperkalemia is associated with usage of digoxin. This is due to the blocking action of digoxin on the Na/K ase which results in accumulation of extracellular K+.
Most of the times, patients presenting with heart problems are already on diuretics before they are prescribed with digoxin. Diuretics cause hypokalemia as they result in excessive excretion of K+ from the body. Hypokalemia in turn causes digoxin toxicity. Digoxin toxicity does not cause hypokalemia, but hypokalemia can worsen digoxin toxicity. |
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Lysosomal storage diseases
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Nieman-Pick(s) (s)phingomyelinase
(G)aucher (G)lucocerebrosidase Tay-sachs TSH Hexosaminidase A GM2 gangliosides Fabry a-Galactosidase A glycolipids |
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Illusions Delusions Hallucinations
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Illusions
Inaccurate Interpretation of an actual outside stimulus, for example: interpret a rope as a snake Delusions Fixed, false beliefs ( false idea) not accepted by the culture, (religion is not delusion, it is beliefs of a particular culture or society) for example: aliens are invading earth Hallucinations Sensory perceptions in the absence of outside stimuli. for example: dog in the room, while no dog at all |
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Urachal duct abnormalties
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Patent urachus vesicourachal diverticulum
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Heart tube
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The Little Orphan Annie tumor
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you can think of papillary thyroid carcinoma as the Little Orphan Annie tumor because:
1. It stays around for years and years without getting any bigger (papillary carcinoma is slow growing). 2. It is well-behaved and seldom kills people (overall, the 10-year survival for papillary carcinoma is >90%, which is better than the prognosis of any of the other types of thyroid carcinoma). 3. The nuclei resemble Little Orphan Annie’s eyes. 4. It often has psammoma bodies (derived from the Greek psammos, or sand): Annie’s dog is named Sandy |
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Formation of secondary retroperitoneal organs
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Prekallikrein XII kallikrein kinninogen positive feedback
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Coagulation pathway
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Coagulation tests
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PT aPTT TT
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Pemphigus vs. Pemphigoid (flaccid bullae vs. tense bullae)
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Both diseases are characterized by bullae (big, blister-like skin lesions)
Pemphigus vulgaris blistering disorders caused by autoantibodies against epidermis, which lead to disruption of the intercellular junctions (and hence bullae). Pemphigus vulgaris is the most common type of pemphigus (“vulgar-” comes from the Latin vulgaris, meaning the general public). It occurs primarily in adults between the ages of 30 and 60, and is characterized by big, flaccid bullae that burst easily (in most patients, you’ll see more ruptured, scab-covered bullae than intact ones). Patients often present first with oral bullae and ulcerations, and later develop bullae on the skin. autoantibodies against desmogleins, which disrupt the connections between the squamous cells of the epidermis and cause very superficial, intraepidermal, fragile bullae. If you do immunofluorescence on the skin, you’ll see a kind of outlining of each individual epidermal cell (because there are autoantibodies bound to the junctions between the cells). Treatment consists of immunosuppressive agents; prognosis is variable, but many patients have a higher than normal mortality rate. Bullous pemphigoid This disease is called pemphigoid rather than pemphigus, because it looks like pemphigus but really isn’t! Pemphigus is characterized by autoantibodies against the connections between epidermal cells. In bullous pemphigoid, patients have autoantibodies – but they are against the basement membrane of the epidermis, not against epidermal cell junctions. This means that the bullae are actually subepidermal, so they are less fragile than those of pemphigus vulgaris (if you see a patient with bullous pemphigoid, you’ll see lots of intact, tense bullae, rather than a bunch of ruptured bullae covered with scabs). The immunofluorescence pattern is correspondingly different – you’ll see just a line at the base of the epidermis (rather than the lace-like outlining of epidermal cells you see in pemphigus vulgaris). Patients with bullous pemphigoid are generally elderly, and the clinical presentation varies a lot (but usually it doesn’t start in the mouth, like pemphigus vulgaris). It’s a less serious disease, usually, since the bullae often don’t rupture (so there’s less chance of infection and scarring). So if you can remember that pemphigus is a disease that has intraepidermal antibodies, then you can keep the clinical presentation and immunofluorescence pattern of the two diseases straight. |
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Hashimoto’s thyroditis
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Anti-TPO is specific while anti-TSHR anti-thyroglobulin present both hashimoto and grave’s
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Cold shock vs. warm shock
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“暖休克”较少见，仅是一部分革兰阳性菌感染引起的早期休克表现。"冷休克"较多见，多由革兰阴性菌感染引起；而且革兰阳性菌感染的休克加重时也成为"冷休克"。
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M1 and M3 receptor
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All glands are M3 except M1 which on GI gland ( cause H+↑). M3 one blood vessel (activate NO synthase) no effect of Ach esterase inhibitor
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Acetazolamide
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causes Hypokalemia -because Of incease in aldosterone release which is stimulated by the diuretic effect of acetazolamide. Aldosterone exchange Na+ for K+(excreted) in CT. Be careful though acetazolamide also cause ACIDOSIS by loss of HCO3- in urine...bcs HCO3- cant diffuse across membrane.
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naloxone methadone naltrexone
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naloxone opiate antidote (repiratory inhibition) u antagonist iv irreversible
methadone (美沙酮) maintenence of opiate addiction u agonist naltrexone alchohol and opiate addiction u antagonist long-acting |
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ACE inhibitor and Diabetes, renal artery stenosis
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AT II contracts both the afferent and efferent arteriole. However, it contracts efferent more than afferent. This leads to ↓perfusion ↑GFR So, in a diabetic that still does not have renal impairment, ACE inhibitors ↑ perfusion, but would ↓GFR if there were no compensatory mechanisms... But, as it exists, ACE inhibitors ↑ perfusion and don't change GFR, what is perfect to diabetic because its nephropathy is due to microvascular insufficiency.
In renal artery stenosis patient, ACE inhibitor cannot ↑perfusion, but cause the dilation of efferent arterioles, ↓GFR Because of this, ACE inhibitors are indicated to Hypertension and Diabetes coexistence, but contraindicated when there is Renal Insufficiency. Because even though ACE inhibitors increase overall kidney perfusion, they decrease glomerular perfusion. That's great in something like diabetic nephropathy where glomerular hypertension is accelerating the glomerulosclerosis - but it could be dangerous in something like bilateral renal artery stenosis, where the atII-constricted efferent arteriole is the only thing maintaining the glomerular pressure that is needed to maintain renal function. But Dr. Raymond said the mechanism of protective role of ACE inhibitor is not clear From WIKI: Renal impairment is a significant adverse effect of all ACE inhibitors, but the reason is still unknown. Some suggest it is associated with their effect on angiotensin II-mediated homeostatic functions, such as renal blood flow. Renal blood flow may be affected by angiotensin II because it vasoconstricts the efferent arterioles of the glomeruli of the kidney, thereby increasing glomerular filtration rate (GFR). Hence, by reducing angiotensin II levels, ACE inhibitors may reduce GFR, a marker of renal function. To be specific, they can induce or exacerbate renal impairment in patients with renal artery stenosis. This is especially a problem if the patient is concomitantly taking an NSAID and a diuretic. When the three drugs are taken together, there is a very high risk of developing renal failure. |
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Insulin resistance and hyperlipidemia
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insulin resistance cause activation of hormone sensitive lipase, then release free fatty acid, increase the liver uptake of FFA, TG synthetic rate increase.
Insulin resistance cause decreased activity of LPL, reduce the degradation of VLDL |
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thiazide and nephrogenic diabetes insipidus
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the diuretic hydrochlorothiazide (a thiazide diuretic) or indomethacin can improve nephrogenic diabetes insipidus. Thiazide diuretics are sometimes combined with amiloride to prevent hypokalemia. It seems paradoxical to treat an extreme diuresis with a diuretic, but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering GFR and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained
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How can hypercalcaemia and hypokalaemia leads to polyuria?
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TAL: 1 Na+, 1 K+ and 2 Cl- cotransporter
This is the major way that Na+ is absorbed in this area (but not the major way overall - most sodium is reabsorbed much earlier). However, there is a problem: there are much less K+ than Na+ ions, and if K+ runs short, the pump doesn't work. The body gets around this by allowing some K+ to leak back from the cell (where it's just been transported) into the tubular lumen again. Thus, the pump can continue to operate. Already, the mechanism of polyuria in hypokalaemia is obvious. If there is low potassium in the blood, there will be low potassium in the tubules (since tubular fluid is an ultrafiltrate of blood). And if there is low potassium in the tubular fluid, there won't be enough to allow the 1Na+/2Cl-/1K+ pump to work (even if some does leak back into the lumen). With less Na+ absorbed due to the above pump's failure, there is more Na+ in the tubular lumen. And since Na+ is so osmotically active, water is retained alongside it: polyuria. A similar thing happens in the collecting tubule later one (this time with a Na+/K+ pump). And hypercalcaemia? The high tubular concentration of calcium makes the net charge of the tubular fluid more positive (Ca2+). This tends to inhibit the back-leak of K+ ions, since they are also positively charged, and 'like' charges repel. Again, this inhibits the above pump, resulting in more Na+, and thus more water, in the lumen. (It isn't due to osmolarity, as the above answerer writes: Ca2+ isn't very osmotically active). Compounding both of these states (hypercalcaemia and hypokalaemia) is the odd fact that the kidney also responds less well to ADH. Thus both of these states are causes of 'nephrogenic diabetes insipidus', but the jury's still out on quite why. Regardless, this makes the polyuria worse. |
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cardiac cycle
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