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UWorld Endocrine Flashcards

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USMLE® Step 1 flashcards
1
Q

In Graves, what does B blocker NOT fix?

A

Exopthalmos. B blockers may fix mood lability and fatigue - stemming from symapthetic overactivation. B BLOCKER ALSO BLOCKS PERIPHERAL CONVERSION OF T4 TO T3.

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2
Q

What is one of the most common reasons for elevated alpha fetal protein?

A

AFP synthesized by fetal liver, GI tract, and yolk sac.And thus AFP INC w/ gestational ageMost common reason for INC/DEC AFP levels is gestational age.

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3
Q

Klinefelters - What are…LH, FSH, Estrogen, Testosterone, Sperm count?Turners?

A

LH, FSH, Estrogen are INC, Test, Sperm DEC.Turners, Estrogen DEC (streak ovaries), which leads to LH and FSH INC.

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4
Q

Thiazolidinediones mech of action? Aka pioglitazone (glitazone)

A

Bind to peroxisome proliferator actiavted receptor gamma (PPAR) , a receptor that belongs to steroid/thyroid superfamily of NUCLEAR RECEPTORS - Basically skips the external insulin binding and DECREASES insulin resistance and INCREASE INSULIN SENSITIVITY IN PERIPHERAL TISSUES!!PPAR gamma codes for adiponectin - cytokine secreted by fat. Low in DM2. TZD INC levels. DEC insulin resistance.

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5
Q

In septic shock - what plasma findings are different?

A

Lactic acidosis - INC anion gap - due to tissue hypoxia - results in impaired oxidative phosphrylation. pyruvate shunted to lactate -> hepatic hypoperfusion also contributes to buildup of lactic acid, as liver is priamry site of lactate clearance.

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6
Q

exposure to radioactive heavy isotopes disposal - what to do?

A

Give Potassium Iodide.May prevent thyroid absorption of radioactive iodine by competitive inhibition

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7
Q

Medication of choice for Gestational DM?

A

Insulin

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8
Q

Mech of action of finasteride?

A

5 alpha reducdtase - knocks out peripheral converison of T to DHT. Finasteride - used to treat BPH - also can tx andorgenetic alopecia. (Can give you hair)

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9
Q

How is fructose metabolized in essnetial fructosuira?

A

Essential - fructokinase deficiency - In this case, fructose is metabozlied by hexokinase to F6P. This pathway is not significant in omral individuals

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10
Q

Mech of menopause? Most reliable test way to confirm?

A

Estrogen (estradiol, NOT estrone - remains normal from fat), DEC leading to INC FSh and LH. INC FSH are the gold standard for determining menopause

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11
Q

Transmembrane domains are composed of?

A

Hydrophobic amino acids. (valine, alaniem, isoleucine, methionine, phenylalanine. AKA inside, they are shielded from direct contant w/ water.

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12
Q

Kallmann syndrome - where is the defect? What is the presentation?

A

Abscence of GnRH. Delayed puberty+ anosmia. Failure of GnRH secereting neurons to migrate from origin in olfactory placode - to normal often due to KAL1 mutation or fibroblast grotwh factor receptor 1 gene. location in hypotahalmus.

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13
Q

What is a crossover study? What is a wash out period?

A

Crossover - give A then B to one group.Give B then A to another.In between A and B have a no treatment period to “wash out” any effects.

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14
Q

Where are thyroid hormone receptors?

A

Inside nucleus.

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15
Q

Tx for adrenal crisis?

A

Corticosteroids

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16
Q

Histo of bone in hyperparathyrroidism?Caused by? Presentation?

A

Subperiosteal thinning w/ cystic degeneration. ESP on medial side of second and 3rd phalagnes of the hand. Cuased by a parathyroid adnemoa in 85% of pt. Parathyroid CA is VERY uncommon. Often see bones, stones (RENAL COLIC) groans, psychic moans, + GI upset (ULCERS)

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17
Q

Histo of hashimotos?

A

Mononucelar parenchymal inifiltration w/ WELL DEVEOD GERMINAL CENTERS - classic Hahsimotos.

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18
Q

How can you tell where damage in central diabetes insipidus is at?

A

Give ADH and see response over time. If damage is to posterior pit - transient Central DIPermanent central DI - dmg to hypothalamic nuclei or pituitary stalk.

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19
Q

Best diabetes t2 tx for post-meal?

A

Any rapid acting.Lispro, aspart, glulisine.However, Lispro is IV so probably others.

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20
Q

What is the pharm remediation for anovulation?What are the two drugs used - for what reasons?

A

Menotropin (acts like FSH) - leads to formation of dominant ovarian folliclehCG (simulates LH surge) - leads to ovulation.

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21
Q

Removal of mass in infants neck leads to lethargy, feeding problems, constipation, dry skin.Why?

A

Removal of lingual thyroid - sometimes this may be the ONLY thyroid that the child has - leads to hypothyroidism. See all these in infants + umbilical hernia macroglossia etc.

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22
Q

Where are NADH, GTP, and FADH synth in TCA cycle?What is the GTP used for?

A

NADH - isocitrate to akGNADH - akG to succinyCoAGTP - Succinyl Coa to SuccinateFADH - Succinate to FumarateGTP is used in glucoNEOgenesis for the phosphorylation and decarboxylation of oxaloacetate to PEP by PEP carboxykinase.

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23
Q

What 2 things stimulate the pancreas to release enzymes and bicarb? Which cells do these affect?

A

CCK -> Acinar -> EnzymesSecretin -> Ductal -> BicarbCAESDB

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24
Q

How does glucose get from lumen into cell.

A

NaK pump establishes gradientNa/Glucose flow into the cell togetherGlucose flows out of basal side via facilitated diffucsion.

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25
Q

Another name for facilitated diffusion?

A

Carrier mediated transport. These are transmembrane carrier proteins.

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26
Q

Other than Agranlocytosis, Aplastic anemia, hepatotoxicity, teratogenesis, Steven Johnson and p450 induction, what can this drug lead to (endocrine)?

A

SIADH - by exaggerated response to ADH. Carbamazepine - Na inativation.

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27
Q

Where does ADH synthesis occur? Oxytocin synthesis?Where is this all secreted into?

A

Supraoptic nucleus. Perhaps tie this in with seizures/carbamazepine, which can cause SIADH and seizures, which can? cause you to see shit. Paraventricular nucleus Secreted into hypophysial vein - ultimately enterse systemic circulation. Hypophysial vein is in between psoterior and anterior pit.

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28
Q

What is the DOC for DKA?

A

regular

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29
Q

What ist he most common cause of death in pt w/ DM?

A

Cornoary heart disease/MI.Studies show that DM is one of the strongest risk factors for CHD. Approx 40% of pt die secondary to CHD. Exceeds risk of dying to renal failure, stroke, hyperosmolar nonketotic coma.

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30
Q

Hyperthyroid pt w/ fever. Must?

A

Get WBC.Fever - concern for agranulocytosis (absolutle N count less than 500/mL.)Also may present w/ fever + THROAT PAIN/SOARE THROAT.

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31
Q

Antithyroid drugs.3 types:Anion inhibitorsThianamidesRadioablationIodide Salts

A

Anion inhibitors - perchlorate, pertechnetate (comeptitive inhibition)Thionamides (methimazole, PTU - inhibit thyroid peroxidase)RadioablationIodide Salts - potassium idodie -0 inhibit synth and release

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32
Q

What have Glut 2 receptors?Glut 3 receptors?

A

G2 - Liver, pancreatic b cells, intestine, kidneysG3- placenta, brain, neuron

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33
Q

Where are cortisol receptors located?

A

Within cytoplasm - translocate to nucleus after binding to cortisol.

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34
Q

What can induce insulin resistance?What is the mech of this?

A

TNFa - Catecholamines, glucocoritcoids, glucagon - INC serine kinase activity - lead to phosphorylation of IRS-1 (insulin receptor sbustrate) - this inhibits IRS1 tyrosine phosphorylation of insulin.

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35
Q

Why does prolactinoma lead to other signs other than bitemporal hemianopsia?

A

Inhibits GnRHMales - low LH, T - impotence, usu no galactorrhea or amenorrheaFemales - low LH, estrogen - galactorrhea, amenorrhea - may lead to osteoporosis due to low E.

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36
Q

ACTH - hyperplasia of what?

A

Fasciulate (cortisol!)ACTH IS NOT ALDOSTERONE, IT IS CORTISOL! DUHHHHHHH

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37
Q

SIADH plasma findings, fluid levels?

A

Low sodium and osmolality - inappropriate concentrated urine - INC urinary sodium - CLINICALLY NORMAL BODY FLUID - NO edema - no lung fluid build up, JVD etc. No fluid problems because ADH is corrected as extracellular fluid SUPPRESSES renin-aldosterone - and stimulates Natriuretic peptides - leading to excretion of sodium in urine - EUVOLEMIC HYPONATREMIA.

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38
Q

Glucose, Galactose, Fructose - fastest rates of gylcolytic metabolism?

A

Fructose - it bypasses regulatory step of PFK1. And goes directly to Aldolase B

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39
Q

B blockers concern w/ diabetes?

A

Nonselective B blcokers exacerbate hypoglycemia and MASK ITS ADRENERGIC SYMPTOMS - should not be use din pt w/ DM unless benefits outweight concenrs.Selective B1 antagonists hsould be used isntead if necessary. Block of B2 inhibits hepatic gluconeogensis and peripheral glycogenolysis/lipolysis. B1 blockers are given because they do not block metabolic sympathetic effects.

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40
Q

In MEN 2a syndrome - which cells of the thyroid are affected? Which cells of the adrenals?

A

Parathyroid - Medullary thyroid CA - PARAFOLLICULAR cells (C cells!) - which release Calcitonin. PheoBoth parafolliclular and Pheos (adrenal medullary - aka chromafin, whiy you have catecholamine release) are neural crest derivatives.

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41
Q

What are the two a-glucosidase inhibitors. When are they taken?

A

Acarbose, MiglitolTkane with meals for maximal effect - side effects - GI upset. Dont use in pt w/ malabsoprtion.

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42
Q

What effect would giving T3 have on T4 and rT3?

A

Giving T3 would DEC TSH, which would DEC T4, which would DEC rT3REMEMBER - rT3 is made from T4! not from T3.

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43
Q

Why does the zona glomerulosa only may mineralocorticoids (aldosterone)

A

Because it does not have 17a hydroxylase. Cannot make cortisol or androgens.

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44
Q

Describe the polyol pathway.Why do you get cataracts, retinopathy, neuropathy in DM and other sugar disease?

A

Glucose - aldose reductase -> SorbitolSorbitol -> sorbitol dehydrogenase -> Fructose.Retina, Schwann cells, Kidney have aldolase reductase, but DONT have sorbitol dehydrogenase.Lens DO have sorbitol dehydrogenase, but after a while in DM this can get oversaturateed. Think - “lens is most protected (has both enzymes) since it needs to be clear, but eventually even this goes” So probably have retinopathy before lens problem.

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45
Q

What effect does anastrozole have?What is another drug in this same category?

A

Aromatase inhbiitor - used in postmenopausal women w/ breast CAAnastrozole and Exemestane are both aromatase inhibitors.

46
Q

What is the most efefctive prevention intervetion in a diabetic smoker, with hx of hypertesnion

A

Stop smoking.Even though CAD is most likely cause of death in DM patient..

47
Q

In men w/ one testicle, what are the usualy FSH, LH, T, Findings?

A

1 testicle means significant loss of mass of Sertoli cells - therefore, circulating inhibit B levels are low. Since these levels are low, you have INC FSH secretion from ant. pit. Leydig can uus compensate so you have normal LH, and thus normal T, DHT

48
Q

What is DHEA?

A

Precursor to T and DHT. Also weakly androgenic by itself.

49
Q

How does GH stimulate linear growth?When can you have linear growth deficits w/ normal/high levels of GH?

A

Via production of IGF-1 from the LIVER.Laron dwarfism - normal/high GH in the presence of low IGF-1 (due to DEFECTIVE GH RECEPTORS!)

50
Q

What to always check before starting metformin?

A

Kidney function - Meformin - INC insulin sensitivity, DEC gluconeogenesis. And thus, MORE lactic acidosis ()anaerobic glyoclysis)Lactic acidosis can be complicated by kidney dysfunction.

51
Q

Cause and Treatment for hirsutism?

A

Usu from INC T or T->DHT.May occur during Polycystic ovary syndrome for these very reasons (INC T) Tx w/ spironolactone. Also flutamide (inhibits binding to T receptors) and finasteride (5-alpha reductase inhbiitor)

52
Q

What does methylation of DNA lead to?

A

formation of HETEROCHROMATIN (collection at periphery of nucleus) and low transcirptiona activity.Remember, histone acetylation -> activation.

53
Q

What does a BARR body appear like?

A

inactivated X chromosome - usually found in the periphery of the nucelus.

54
Q

Metyrapone - what does it do? When is this test used? What excretion product will you see after administration?

A

Metyrapone - used if suspicious of HPA dysfunction. Metyrapone - blocks 11 B hydroxylase - is lead to DEC cortisol. DOES NOT AFFECT ALDOSTERONE PATHWAY - slightly different pathway. Also If you DEC cortisol -> INC ACTH/ACTH surge. If HPA axis is normal - significant INC in 11 deoxycortisol in serum and 17 hydroxy-corticosteroids in URINE.

55
Q

When do liver glycogen stores become depleted? After glycogen depleted, how are blood glucose levels maintained?

A

Usu after 12 to 18 hours of fasting.After glycogen depletion, gluconeogenesis is the primary process of keeping blood glucose up.So in 24 hour fast - it’s gluconeogenesisPyruvate -> OAAOAA -> PEPCreate glucose w/ either OAA or PYRUVATE.

56
Q

Where (2) do you find glucokinase? What is its role?

A

Found in pancreatic beta cells and liver - glucose sensor.Inactivation of enzyme results in mild hyperglycemia that is exacerbated by pregnancy.

57
Q

Pt w/ BUN of 75 and Cr of 5.8What are parathyroid levels and Ca levels?

A

Pt is in renal failure.Therefore 1-a-hydroxylase isnt working as well, and low vit D.Therfore low Ca + INC PTH. (secondary hyperparthyroidism)

58
Q

Normal urine osmlality after dehydration in Normal ptNeurogenic DINephrogenic DIPrimary polydipisa

A

Norma - more than 800Neurogenic less than 300Nephrogenic 300-500Primary polydipsia more than 500.In normal and primary polydipsia, giving Vasopressin will have little affect BECAUSE this system is already working fine. Less than 10% INC in urine osmolarity post injection.

59
Q

Differentiate types of tyrosine kinasesWhat are their signaling pathwaysWhat are examples of both types?

A

Intrinsic enzyme activity - Receptor tyrosine kinase –>Have cytosolic enzymes. –> MAP-kinase. Receptor autophosphorylation of Ras. Examples Growth factor receptors: EGF, PDGF, FGF.________________Without intrinsic enzyme activity (tyrosine kinase associated receptors) - cytosolic domain but NO enzymatic activity - JAK/STAT – receptors for cytokines, GH, prolactin, IL2.

60
Q

What substances utilzies JAK pathway?

A

Nonenzymatical activit - JAK/STATGH, cytokine receptors, prlactin, IL2.

61
Q

What is the most important determinant of inuslin resitance?In women and men.

A

Visceral obesity - waist to hip ratio.

62
Q

What is the mech of infiltrative opthalmopathy in graves.

A

Infiltartion of lymphocytes into extrocular muscles and connective tissue. CYTOKINSE from Th1 stimulate retro orbital fibroblasts to secrete glycosaminoglycans.Therefore, tx w/ glucocorticoids is effective.

63
Q

Description of craniopharyngioma?

A

CalcificationsCysticCholesterol crystals (fluid rich in cysts)

64
Q

DM, necrolytic erythema, anemia

A

GLUCAGONOMA - Rare pancreatic tumors - w/ these 3 findings. Also elevated erythematous rash in groin area.

65
Q

Pt w/ anorexia nervosa that experience amenorrhea -w here is the defect in?

A

GnRH from hypothalamus - loss of pulsatile secretions. Starts at the top. Can lead to osteoporosis due to downstream low levels of estrogen.

66
Q

Early virilization 2-4 years old - think? Other presentations of this?

A

21-hydroxylase def Classic, salt wasting - present at birth/1-2 weeks w/ hyponatremia, deyhdration, hyperkalemiaClassic, non-salt wasting

67
Q

Tx for pt w/ 21 hydroxlyase def?

A

w/ 21 hydroxylase def, have excessive androgens.Also due to low levels of aldosteron and cortiol, you have excessive levels of ACTH.Give these pt. low dose exogenous corticosteroids to suppress excessive ACTH and therefore reduce stimulation of adrenal cortex.

68
Q

What does positive skew/negative skew look like?

A

Positive skew - mroe towards the left. Mean>median > modeNegative skew - more towards the right. mean

69
Q

Reaction wise.. B1 think? ThiamineB7 think? Biotin

A

B1 - Minus CB7 - Plus C (carbon carrier)B1 makes Pyruvate -> AcetylCoAB1 makes - akG (5) -> SuccinylCoAB7 - Proprionyl CoA (3) -> Methylmalonyl CoA (4)B7 - Pyruvate(3) to OAA(4)

70
Q

What would lead to biotin deficiency?

A

Excessive consumption of egg whites.

71
Q

Adiponectin?Relation to PPAR? Effect of glitazones?

A

PPAR -> Adiponectin (Cytokine secreted by fat). Low in DM2. Glitazones - INC insnulin sensitivity by binding to PPAR.INC adiponectin, INC insulin receptor substrate, INC GLUT4.

72
Q

What DM drug would INC C-peptide levels?

A

Glyburide (any Sulfonylurea)Due to release of ENDOGENOUS insulin.

73
Q

What should be monitored periodically w/ pioglitazone administration?

A

Hepatotox - LFTs. Also known to induce fluid retention - can exacerbate CHF (contraindicated in NYHA class 3 and 4)

74
Q

How to diff against 21 hydroxylase and 11 hydroxylase def?

A

11 hydroxylase still builds aldosterone precursor - will have hypertensiom/hypernatremia/hypokalemia in baby.

75
Q

Where are epi, norepi, dopa produced?How is Epi made and released? What affects this?

A

NE, Dopa = mainly CNS and PNSEpi is mainly adrenal glands. Conversion of NE to Epi occurs in adrenal medulla by phenylethanolamine N methytransferase )PNMT)CORTISOL INC transcirption of PNMT. Hormal medulla contains 80% Epi, 20% NE due to all the upregualted PNMT from cortisol.

76
Q

What enzyme does muscle lack that liver has?

A

Glucose 6 phosphatase.Cant take G6P and make it into glucose. Muscle uses G6P for its own glycogen needs.

77
Q

Describe the insulin activation pathway of hepatocytes etc.

A

Insulin -> tyrosine kinase -> activates Protein Phosphatase-1 -> modulates acitivty of enzymes .

78
Q

Well developed SER - think?

A

Lipid, steroid, phospholipid biosynthDetox.All steroid producing cells (adrneals, gonads, liver) contain well devos SER. Example ACTH.

79
Q

What serum findings are thought to INC insulin reistance in overweight individuals (dont say prolonged glucose exposure)

A

FFA and serum triglycerides - thought to INC insulin resistance.

80
Q

Effect of estrogen on thyroid hormone stuff?

A

Estrogen leads to INC in TBG, and thus INC total T4 and total T3.However, free thyroid is normal (euthyroid)Also seen in oral contraceptives, and hormone replacement therapy

81
Q

What are the effects of TZD (thia-zolidine-dione) on andiponectin?

A

Adiponectin low in T2 diabetes.Tx w/ TZD INC levels of adiponectin - and of course INC transcription modulation leading to DEC insulin resistance and INC insulin sensitivity.

82
Q

PT w/ DM 1 at risk for?

A

Other autoimmune - hashimotos, Graves, addisons (hypoadrenocorticism) Also Pernicious anemia and vitiligo

83
Q

What serum changes do you see in DM1 pt w/ ACTH stim test failing to produce cortisol?

A

Primar yadrenal insufficiency - see more than just Cortisol defect. Also have Aldosterone problem etc.So DEC Na, INC K, DEC Bicarb, DEC Cl. (no aldosteron - metabolic acidosis) Addisions disease has def of ALDOSTEORN ENAD CORTISOL.

84
Q

Excessive insulin WITH Appropriately high C peptide? What pharm can do this?

A

Sulfonylurea - INC endogenous release. Sulfonylurea close K channel - depol cell - Ca influx -> Insulin release. Careful of hypoglycemia nad other side effects. Useless in DM T1. No insulin to release.

85
Q

Only way to differentiate between insulinoma and sunfonylurea or meglitinide abuse?

A

All have INC c peptide, proinsulin, serum insulinWould have to screen the urine or blood for hypoglycemic agents.

86
Q

What is DM T1 diagnosis made off of?

A

Fasting blood sugar levels.NOT ORAL GLUCOSE TOLERANCE TEST = this is usu ussed to screen pregnant women for gestational DM. Fasting blood glucose is the perference for DM T2 tests too.

87
Q

DM T1 first presentation?

A

Can be acute or subacute - often tirggered by “recent viral infection” in young caucasian adult. (early 20s)

88
Q

What serum levels can be up in MEN2 or 3?

A

Calcitonin! Dont forget medullary CA of thyroid is in medulalry parafollicular C cells! (calcitonin producing!)+ perhaps epi/noreepi - from pheo

89
Q

Concerns w/ amiodarone treatment.Screen first for?Screen while using for?

A

Amiodarone - Screen first - Thyroid levelsScreen while - Pulmonary fibrosis, thyroid dysfunction, corneal deposits (common), blue/purple skin. Amiodarine is 40% iodine by weight! May induce hypothyroidism -> Tx w/ levothyroxine and keep using amiodarone.

90
Q

Most common pitutiary adenoma?

A

Prolactinoma (from lactotroph cells)Even though somatotrophs are the most common CELL TYPE (Growth hormone)

91
Q

What are neurophysins?

A

Carrier proteins for oxytocin and ADH. Act as chaperone molecules to shuttle them towards posterior pituitary. Point Mutations in Neurophysin II can cause AD heredtiary hypothalamic Diabetes Insipidus.

92
Q

Where is MEN 1 gene located? RET?

A

MENIN gene - Chr 11. MEN 2,3 - RET gene Chr 10

93
Q

Jejunal ulcer - think?

A

Gastrinomas.Usu more common ulcers are duodenal.

94
Q

What are the symptoms of a VIPoma?Tx?

A

Watery Diarrhea, Hypokalema, Achlorhydria (WDHA syndrome) also vasodilation (flushing), hyperCa, Hyperglycemia. VIP inhibits gastrin -> blocks acidOcreotide (somatostatin)

95
Q

In terms of thyroidRET ->RAS -> p53 ->

A

Nothing - PapillaryRAS - Follicular RET - medullary thyroidp53 - anaplastic

96
Q

Risperidone side effects?

A

Hyperprolactinemia - cause amenorrhea, galactorrhea, breast soreness/tendernessRisperidone has anti-dopamine action - INC prolactin secretion.

97
Q

Slow deep tendon reflexes + dry coarse skin?

A

Hypothyroidism.likewise, FAST deep tendon - hyperthyroid.

98
Q

Fatigability, weight gain, elevated CREATINE KINASE?

A

Hypothyroidism - specifically - hypothyroid myopathy -Biopsy may show muscles w/ pale muscle fibers w/ DEC striation and deposition of mucinous material.

99
Q

Indications for flutamide? Mech?

A

Flutamide - used for prostatic CA.Mechanism - nonsteroid- antiandrogen. Competes w/ T and DHT for receptors. AKA DEC stimulatory efet of androgens on primary tumor and metastases.

100
Q

Primary hyperaldosteronism - what are the lab values of Na, K, Bicarb?

A

Na - normal! (aldosterone escape)K DECBicarb INC

101
Q

What is aldosterone escape?

A

When you have INC Na and CL absorption, you get HYPERVOLEMIC - which leads to ANP release and thus diuresis and compensatory sodium loss. ANP causes DEC Na reabs at renal collecting tubule - so basically anti-aldosterone, and also cGMP dilates afferend and constricts efferent, leading to INC diuresis.

102
Q

Mech and Side effects of Thiazolidinediones?

A

DEC insulin resistance by binding peroxisome proliferator acitvated recpetor (PPAR) - fluid retention/weight gain/precipitates CHF. Also HEPATOTOXICITY - must monitor LFTS.

103
Q

Mild flu like illness few weeks ago. Mood swings, hand tremor, Pain in neck, INC ESR, high blood pressure. What is this, what does histo look like?

A

This is DeQuervains ThyroiditisHisto - GRANULOMATOUS INFLAMMATION - MIXED CELLULAR INFILTRAT W/ OCCASIONAL MULTINUCLEAR GIANT CELLS. HYPOTHYROIDISM THAT may BE HYPERTHYROID early on due to destruction.

104
Q

What is pituitary apoplexy?

A

Hemorrhage of preexisting pituitary adenoma. Sudden severe headache and cranial enrve paralysis, + other chronic symptoms of pituitary tumor. hemianopsia, DEC libido, Cardiovascular collapse may occur due to adrenocortical deficiency.

105
Q

What does permissive mean on describe effects of one active substance on anther?What is tachyphylaxis?

A

For example -c ortisol does not have direct effect on vascular reacitivty. Auguments vasoconstrictive EFFECTS of catecholamines. It is not synergistic of additive because it had no effect on its own. INC responsiveness to something = permissive. Tachyphylaxis - DEC drug responsiveness w/ repeat administration (NO, amphetamines, DDAVP, hydralazine, caffeine)

106
Q

In non medical situations, what is given to treat L.O.C. due to hypoglycemia?Medical setting?

A

Nonmedical - IM glucagon - works on liver to INC glycogenolysis and gluconeogenesis (NOT epi)Medical - IV dextrose.

107
Q

SLE pt who is being tx for the disease. What would their adrenals look like?

A

BIlateral cortical atrophy.exogenous Cortisol depresses HPA axis. If taken of exogenous, would go into adrenal crisis.

108
Q

How to differentiate Follicular adenoma from Follicular thyroid cancer HISTO?

A

FTC would have capsular and ascular invasion.

109
Q

In water suppression test, what suggests central DI?complete vs partial central DI?

A

More than 10% INC in urine osmolality following ADH administration suggests central DI (this means that kidney IS responsive to ADH, it’s just not getting it)More than 50% INC in urine osmolality suggests COMPLETE central DI (INCREASES a lot because it produces NONE)

110
Q

Which DM (1 or 2)Has strong HLA class 2 makeup?AMyloid deposition?

A

DM1 - HLA class 2 DM2 - genetic component overall tho. DM1 - 50% concordance in identical twins .DQ2,8DM2-80% oncordance in identical twins. DR3,4DM2 - Pancreatic islet amyliod deposition - amylin is thought ot be a factor that may lead to beta cell dysregulation in DM2. IS ALMOST UNIVERSAL in pt w. DM2.

111
Q

Patients w/ pyruvate dehydrogenase deficiency - what is the problem seen?

A

Cant do pyruvate -> Acetyl coApyruvate shunted to lactic acid (LACTIC ACIDOSIS)Give LYSINE AND LEUCINE - as these are EXCELUSVIELY KETOGENIC and do NOT INC blood lactate levels.

USMLE (16 decks)

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