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Block 8 > U-World: Other > Flashcards

U-World: Other Flashcards

1
Q

What are the characteristics of a melanoma (remember ABCDE)?

A

Asymmetry
Border irregularities
Color variation (brown/ tan/ black/ red)
Diameter > 6mm
Evolving (lesion changing in size/ shape/ color, or new lesion)

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2
Q

Why might a person with melanoma get seizures?

A

Melanoma can metastasize to the brain.

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3
Q

Melanocytes come from what embryologic origin?

A

Neural Crest Cells (NCCs)

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4
Q

What cells are derived from neural crest cells (NCC’s)?

A 
“MOTEL PASSES”
Melanocytes
Odontoblasts (tooth cell)
Tracheal lining
Enterochromaffin cells (produce catecholamines in the adrenal medulla) 
Leptomeninges (arachnoid, pia) 
PNS ganglia (cranial, dorsal root, autonomic) 
Adrenal medulla
Schwann cells
Spiral membrane (aorticopulmonary septum) 
Endocardial cushions 
Skull bones
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5
Q

What embryo cells are melanocytes derived from?

A

NCCs (neural crest cells)

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6
Q

What embryo cells are odontoblasts (tooth cells) derived from?

A

NCCs (neural crest cells)

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7
Q

What embryo cells is the tracheal lining derived from?

A

NCCs (neural crest cells)

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8
Q

What embryo cells are enterochromaffin cells derived from?

A

NCCs (neural crest cells)

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9
Q

What embryo cells are leptomeninges (arachnoid, pia) derived from?

A

NCCs (neural crest cells)

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10
Q

What embryo cells are PNS ganglia (cranial, dorsal root, autonomic) derived from?

A

NCCs (neural crest cells)

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11
Q

What embryo cells is the adrenal medulla derived from?

A

NCCs (neural crest cells)

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12
Q

What embryo cells are Schwann cells derived from?

A

NCCs (neural crest cells)

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13
Q

What embryo cells is the spiral membrance (aorticopulmonary septum) derived from?

A

NCCs (neural crest cells)

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14
Q

What embryo cells are endocardial cushions derived from?

A

NCCs (neural crest cells)

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15
Q

What embryo cells are skull bones derived from?

A

NCCs (neural crest cells)

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16
Q

What is pleiotropy?

A

When multiple phenotypes (lots of random symptoms) result from a single genetic mutation

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17
Q

What’s the difference between endothelial and epithelial cells?

A

Endothelial cells- cells lining blood vessels

Epithelial cells- cells lining other tissues

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18
Q

What cellular organelle is found both in the cytoplasm and bound to the ER?

A

Ribosomes

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19
Q

Where is mRNA made in a cell? Where is rRNA (ribosomal RNA) made in a cell?

A

mRNA—> in the nucleus

rRNA—> in the nucleolus

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20
Q

What is the inheritance pattern of PKU?

A

Autosomal recessive

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21
Q

Eczemia rash, weird gate, intellectual disability, and musty body odor. What is it?

A

PKU

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22
Q

What do hypohidrosis and hyperhidrosis mean?

A

hypohidrosis- diminished sweating

hyperhidrosis- excessive sweating

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23
Q

What is acetoacetate?

A

a ketone body

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24
Q

How long do you have to fast/ be starving for your body to begin producing ketone bodies?

A

kids–> 8-10 hours

adults–> 1-2 days

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25
Q

What pathway leads to formation of ketone bodies?

A

beta-oxidation (break down fatty acids to make ketone bodies)

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26
Q

What hormone can be given to treat Turner syndrome patients?

A

growth hormone

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27
Q

growth hormone receptors are what kind of receptors?

A

JAK-STAT

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28
Q

If you suspect hyper or hypothyroidism, what test are you going to order?

A

serum TSH

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29
Q

what is hypotonia?

A

floppy baby syndrome

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30
Q

How does hypothyroid myopathy present?

A

Myalgias (muscle pains), proximal muscle weakness, elevated creatine kinase, and delayed relaxation of deep tendon reflexes.
(*other causes of myopathy with elevated creatine kinase include inflammatory myopathies, muscular dystrophies, and HMG-CoA reductase inhibitors)

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31
Q

Patient has bitemporal hemianopsia (loss of peripheral vision) and irregular menses. What is likely to be the problem?

A

Pituitary adenoma compressing the optic chiasm- most likely PROLACTINOMA (since the tumor is secreting prolactin, that inhibits GnRH and can stop a woman from having her period)

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32
Q

What are somatotrophs?

A

cells in the anterior pituitary that secrete GH (growth hormone)

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33
Q

What are lactotrophs?

A

cells in the anterior pituitary that secrete prolactin

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34
Q 
What do the following anterior pituitary cells secrete?
Gonadotrophs
Corticotrophes
Thyrotrophes
Lactotrophes
Somatotrophes
A 
Gonadotrophs--> FSH, LH
Corticotrophes--> ACTH
Thyrotrophes-->TSH
Lactotrophes--> Prolactin
Somatotrophes--> GH
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35
Q

Obese woman with hirsutism and bad periods. what should you think of?

A

PCOS

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36
Q

Most common cause of hirsutism (male-like hair growth) in a woman is what?

A

PCOS

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37
Q

How can oral contraceptive pills treat hirsutism in a woman?

A

By suppressing pituitary LH secretion–> decreased androgen production by the ovaries

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38
Q

What part of the adrenal steroid synthesis pathway does Metyrapone inhibit? Explain the Metyrapone stimulation test.

A

Metyrapone inhibits the last step to make cortisol (11 beta-hydroxylase) from 17-OH.
Metyrapone stimulation test: give Metyrapone. Since that stops production of cortisol, the body will accumulate 17-OH and you pee out more 17-OH. Also, the body will inc ACTH in an attempt to inc Cortisol. If you see increase in ACTH, 11-OH, and urinary 17-OH that means the patient’s hypothalamic-pituitary adrenal axis is intact/ working.

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39
Q

Where is pre-pro-insulin made in pancreatic beta cells? How about pre-insulin? Where is insulin and c-peptide released from?

A

pre-pro-insulin is made in the RER (rough ER).
pro-insulin in the secretory granules.
pro-insulin gets cleaved–> insulin + C-peptides in the secretory granules and it gets released from there by exocytosis.

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40
Q

What hormone regulates the zona fasciculata and reticularis of the adrenal gland? What regulates the zona glomerulosa?

A

ACTH regulates the zona fasciculata (makes cortisol) and zona reticularis (makes androgens) of the adrenal gland. Angiotensin II (from RAAS) regulates zona glomerulosa (makes aldosterone) of the adrenal gland.

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41
Q

What effects will increased ACTH have on the adrenal gland?

A

Excess production of cortisol (from zona fasciculata) and androgens (from zona glomerulosa). This can present as Cushing’s symptoms + irregular periods and hirsutism in women.
*Does not lead to production of excess aldosterone (zona glomerulosa) bc that’s under the regulation of ATII (from RAAS).

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42
Q

Most common cause of hyperthyroidism

A

Grave’s disease

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43
Q

Most common cause of hypOthyroidism

A

Hashimoto’s thyroiditis

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44
Q

What are thyrotropin receptor antibodies (TRAb)?

A

TSH stimulating antibodies seen in Grave’s disease

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45
Q

What does pretibial myxedema mean? How about Graves ophthalmopathy?

A

pretibial myxedema= non pitting edema in the shins. Graves ophthalmopathy= bulging eyes. Both findings specific to Graves disease (most common hyperthyroidism) are due to TSH stimulating antibodies. The shins and eyes have TSH receptors–> increased production of GAGs (connective tissue fluid)–> non-pitting edema in shins and thickening of eye muscles the pushes eyes out of sockets

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46
Q

epinephrine stimulates release of what other hormone?

A

glucagon
(remember, glucagon is all about breaking stuff down for energy in a fasting state, and epi is all about this too bc you want fast energy in a short-term stress situation like running from a bear)

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47
Q

How does renal reabsorption of glucose change in response to insulin?

A

It doesn’t! The kidney PCT reabsorbs nearly all glucose no matter what, independent of insulin. (the only exception to this is T2DM where you have so much excess glucose that it overwhelms the kidney tubules and some goes out into your pee)

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48
Q

In T1DM (insulin deficiency), you have an excess of counter-regulatory hormones. What are these?

A

glucagon, cortisol, and growth hormone
(these 3 hormones usually oppose insulin- they pretty much do the opposite things- so without insulin in the mix, they are unopposed and have a greater effect)

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49
Q

How does 21-OH deficiency (type of congenital adrenal hyperplasia) present?

A 
salt wasting (usually in a baby) and virilization in females 
(you can't make aldosterone or cortisol from the adrenal glands--> shunting to making more androgens. Lack of aldosterone leads to salt wasting)
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50
Q

What is thyroxine?

A

thyroid hormone

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51
Q

Increased pituitary gonadotropin release in a kid would result in what?

A 
precocious puberty 
(gonadotropins include FSH and LH)
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52
Q

What is Waterhouse-Friederichsen syndrome?

A

kid gets Neisseria meningitidis–> sepsis and DIC–> hemorrhagic necrosis of the adrenal glands (bleeding out into the tissue and that destroys the adrenal glands)

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53
Q

kid presents with nuccal rigidity (neck stiffness), fever, vomiting, altered mental status. Has hypotension, Na+ wasting, hyperkalemia, low platelet count. He rapidly develops cardiovascular failure and bleeding from venipuncture sites and passes away. What happened?

A

Waterhouse-Friederichsen syndrome. This means: Neisseria meningitidis (neck stiffness, fever, vomiting, altered mental status)–> sepsis and DIC (bleeding out all over, low platelet count)–> hemorrhagic necrosis of the adrenal glands (bledding out into the tissue and that destroys the adrenal glands) (adrenal glands fail–> no aldosterone–> hypotension, salt wasting, and hyperkalemia).

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54
Q

Patient presents with nodule on left thyroid gland and increased calcitonin levels. What cancer is most likely and what gene mutation goes along with this?

A

Medullary carcinoma (the thyroid cancer where your parafollicular, not follicular cells are affected–> inc calcitonin and dec calcium in the blood). Associated with RET gene mutation.

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55
Q

What 2 endocrine conditions are associated with RET mutations?

A

Medullary thyroid cancer (medullary carcinoma) and pheochromocytoma (tumor of adrenal medulla choffamin cells that produce catecholamines). So MEN 2a and 2b (since these multiple endocrine neoplasias include both these).

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56
Q

What’s the difference between primary and secondary amenorrhea?

A

primary amenorrhea–> you’ve never had a period
secondary amenorrhea–> you had periods but now they’ve stopped (*can be due to hypothalamus, pituitary, ovarian, uterine, or other endocrine disorders)

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57
Q

What transport mechanism does glucose use to get into cells from the blood?

A

facilitated diffusion (does not require ATP, but does require the help of transport proteins, which are the GLUT proteins)

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58
Q

Where is GLUT 4 found?

A

skeletal and adipose cells (muscle and fat)

this is insulin-dependent channels for glucose uptake into cells

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59
Q

Histo of which thyroid cancer can be described as follows? nuclei with cleared centers and calcified bodies.

A

Papillary carcinoma (orphan Annie eye nuclei and psammoma bodies)

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60
Q

Histo of which thyroid cancer can be described as follows? Nests of polygonal cells with Congo red-positive deposits.

A

Medullary carcinoma (Congo-red deposits is referring to amyloid deposits from calcitonin, since this is cancer of the calcitonin-secreting parafollicular cells of the thyroid)

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61
Q

Histo of which thyroid cancer can be described as follows? pleomorphic giant cell nests with occasional multinucleated cells

A

Anaplastic carcinoma (malignant cells don’t look anything like normal thyroid cells)

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62
Q

What should you suspect in a patient taking carbamazepine or cyclophosphamide with low Na+, confusion, and seizures?

A

SIADH
These drugs inc risk for SIADH. Inc ADH–> retain excess water–> dec [Na+] and neuronal swelling, cerebral edema–> mental status changes and seizures

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63
Q

How can a prolactinoma affect the bones?

A

excess prolactin–> more inhibition onto GnRH–> decreased estrogen–> amenorrhea (no periods), vaginal dryness, and inc risk for OSTEOPOROSIS with inc risk of fractures (why? because estrogen dec osteoclast activity, so with less of the protective estrogen, you have more osteoclast activity which means more breaking down of bones)

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64
Q

What are the criteria for diabetes? include fasting glucose, random glucose, and A1c.

A

fasting glucose > 126
random glucose > 200
A1c > 6.5%
(*or oral glucose tolerance test- screening for gestational DM and cystic fibrosis related DM)

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65
Q

How might CKD (chronic kidney disease) affect A1c?

A

CDK–> decreased erythropoietin (since the kidneys make EPO)–> decreased RBCs–> falsely elevated A1c (less RBCs to hold hemoglobin A1c, so those RBCs that are around carrying it will have more glucose bound to it)

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66
Q

How might beta-thalassemia affect A1c?

A

beta thal–> HbA2 gets elevated–> resulting RBCs are prone to hemolysis (so more turnover)–> falsely low A1c

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67
Q

SIADH patients have euvolemic hyponatremia. Explain.

A

SIADH= too much ADH release= too much retention of water. This excess water dec [Na+]= hyponatremia. But, ANP and BNP kick in to

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68
Q

smoker presents with confusion and low [Na+]. What should you think of?

A

SIADH secondary to small cell carcinoma (paraneoplastic syndrome)

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69
Q

Craniopharyngiomas are tumors arising from what embryologic structure?

A

Rathke’s pouch

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70
Q

The anterior pituitary forms from what in embryology?

A

out-pouching of the pharyngeal roof called Rathke’s pouch

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71
Q

What is a craniopharygioma and how might it present?

A

Childhood tumor arising from Rathke’s pouch (out-pouching of the pharyngeal roof that forms the anterior pituitary gland). Present with mass effect and visual defects.

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72
Q

Patient has history of SLE. Presents with HTN, obesity, muscluar weakness, ecchymoses, and hyperglycemia. What is the most likely diagnosis?

A

Cushing’s syndrome (inc Cortisol) probably due to glucocorticoid therapy to treat her lupus
(*note: hyperglycemia is due to the fact that cortisol opposes insulin–> prevents glucose from coming into cells, so more glucose remains in the blood)

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73
Q

Why do we taper patients off steroids (glucocorticoids) rather than just have them stop cold turkey?

A

Sudden discontinuation of steroids can cause adrenal crisis. (Giving exogenous steroids causes the body to produce less endogenous steroids. If we stop them all fast, your body cannot adapt and you are still making less steroids without getting any more from meds.)

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74
Q

Why might a lupus patient develop bilateral cortical atrophy to her adrenal glands?

A

Taking endogenous steroids to treat lupus–> body starts producing less and less endogenous steroids (negative feedback since you’re getting steroids from the meds)–> leads to atrophy over time because the organs are not stimulated as much (you don’t use it you lose it–organs shrink when they aren’t used as much)

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75
Q

Why might MEN 2B patients experience headaches?

A

MEN 2B= multiple endocrine neoplasia consisting of medullary thyroid carcinoma, pheochromocytoma (tumor of the adrenal medulla–> excess catecholamines), and mucosal neuromas (papules on lips and tongue). The excess catecholamines cause increases BP and as a result, headaches from the extra pressure within.

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76
Q

Why can a prolactinoma cause decreased testosterone production and decreased libido in men?

A

excess prolactin–> inhibits GnRH–> less LH–> less testosterone

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77
Q

Will a patient with DKA have increased or decreased K+ within cells? Outside of cells?

A

In cells–> decreased K+
Outside of cells–> increased K+
why? Insulin increases K+ going into cells (due to activation of the Na/K pump). DKA patients do not have insulin, so the opposite is true. Another way to think of it: DKA patients are in a metabolic acidosis, so there’s increased H+ acid outside cells that will come into cells. As a result, more K+ will be brought outside of cells to balance charges (normal- high K+, so possibly hypERkalemia)

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78
Q

What does insulin do to K+ levels?

A

Insulin drives K+ into cells (by stimulating the Na/K pump). That means less K+ is outside of cells in the blood= hypOkalemia.

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79
Q

What weight changes are you most likely to see in a patient with Cushing’s syndrome as a result of ectopic ACTH production from small cell carcinoma?

A

weight loss.
Don’t get fooled…in Cushing’s (excess cortisol) we often see re-distribution of fat–> central fat obesity with striae. However, if the Cushing’s is secondary to cancer, it is more likely that the patient is losing weight from the cancer increasing metabolic demand.

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80
Q

Will you see increased, normal, or decreased levels of the following in a primary hypOthyroid patient? TSH, T4, T3.

A

TSH will be HIGH due to negative feedback.
T4 will be LOW due to the hypothyroidism (underactive thyroid gland).
T4–> T3, so you’d expect T3 to be low too, but not a lot of it is made (you only need a little active TH at once) so even though there’s less T4, there’s plenty of T4 ingredients to make the amount of T3 you need. So oftentimes, T3 levels are NORMAL in hypOthyroid patients.

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81
Q

What is a secretagogue?

A

A substance (like a drug) that causes another substance to be secreted.

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82
Q

If you see elevated insulin but low C-peptide, what does that suggest?

A

exogenous insulin secretion (insulin made in the body by pancreatic beta cells gets released with c-peptide, so if insulin is high, c-peptide would be high too–unless the patient is injecting themselves with insulin)

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83
Q

If you see elevated insulin and C-peptide–> hypoglycemia, what does that suggest?

A

The body is making too much insulin due to an insulin-secreting pancreatic tumor (insulinoma) or an insulin secretagogue (medication that stimulates pancreatic beta cells to secrete insulin, like Sulfonylurea).

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84
Q

What is a VIPoma?

A

A non-beta cell panreatic islet cell tumor that secretes too much VIP (vasoactive intestinal polypeptide). This can lead to watery diarrhea, hypokalemia, and impaired gastric acid secretion.

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85
Q

What’s the most common type of congenital adrenal hyperplasia?

A

21-OH deficiency

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86
Q

A deficiency in the enzyme that catalyzes the following reaction is called what? Progesterone–> 11-deoxycorticosterone.

A

21-OH deficiency (the most common cause of congenital adrenal hyperplasia).

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87
Q

Baby girl presents with ambiguous genitalia and enlarged clitorus (clitoromegaly). Or baby boy presents with salf-wasting and precocious puberty years later. What condition is this?

A

21-OH deficiency (the most common cause of congenital adrenal hyperplasia).

88
Q

How will 17-OH (congenital adrenal hyperplasia) deficiency present?

A

HTN and lack of secondary sex characteristics (Able to make aldosterone but cannot make cortisol or androgens–> shunting to make more aldosterone)

89
Q

What’s the most common cause of death in people with diabetes?

A

Coronary heart disease

90
Q

Would the following labs be increased, decreased, or normal in a patient with primary hyperaldosteronism (due to bilateral adrenal hyperplasia or adrenal adenoma aka Conn syndrome)? Aldosterone, Renin, Na+, K+, bicarb.

A

Aldosterone- HIGH

Renin- LOW (due to negative feedback)

Na+- NORMAL (you’d expect it to be high since aldosterone–> Na+ reabsorption, but it’s usually normal due to “aldosterone escape” (increased ANP decreases Na+ retention so you don’t get hypernatremia and lower extremity edema)

K+- LOW (aldosterone–> you pee out more K+ and H+)

Bicarb- HIGH (aldosterone–> pee out more acid/ H+–> less acid/ alkalosis in the blood which means more bicarb.)

91
Q

What is “aldosterone escape”?

A

hyperaldosteronism–> despite increase in Na+ reabsorption, you don’t get hypernatremia and lower extremity edema because ANP is released and lowers Na+ levels (compensates to avoid volume overload, “escaping” the effects of aldosterone in terms of Na+ reabsorption)

92
Q

Pheochromocytoma affects what cell type?

A

Pheochromocytoma is a cetecholamine- secreting neoplasm arising from the CHROMAFFIN CELLS of the adrenal medulla.

93
Q

What does gynecomastia mean?

A

enlarged breasts in men

94
Q

What does cryptorchidism mean?

A

condition where one or both of the testes fail to descend from the abdomen into the scrotum

95
Q

Man comes in for evaluation bc him and his wife cannot conceive. He has gynecomastia, small testes, and long extremities. What condition should you think of?

A

Klinefelter syndrome

96
Q

What are neurophysins?

A

carrier proteins for oxytocin and vasopressin (ADH)

97
Q

How does Hashimotos look on histology?

A

Chronic inflammation with germinal centers and Hurthle cells (eosinophilic metaplasia of cells that line follicles)

98
Q

Woman presents with fatigue, weight gain, constipation, and enlargement of the thyroid gland. Biopsy shows intense lymphoplasmacytic infiltrate with active germinal centers. What is it?

A

Hashimotos thyroiditis

99
Q

What thyroid condition does this histo description fit? Branching papillae with cells containing empty-appearing nuclei.

A

Papillary carcinoma (orphan Annie nuclei)

100
Q

What thyroid condition does this histo description fit? Dense fibrous tissue extending beyond the thyroid capsule.

A

Riedel thyroiditis (lots of fibrosis in thyroid gland that makes it “hard as wood”)

101
Q

What thyroid condition does this histo description fit? Follicular hyperplasia with tall cells projecting into the follicular lumen.

A

Grave’s disease (elongated epithelial cells and scalloping of the colloid)

102
Q

What thyroid condition does this histo description fit? Widespread inflammatory infiltrates, giant cells, and disrupted follicles.

A

De Quervain thyroiditis (Subactue granulomatous)

103
Q

What does paresthesias mean?

A

tingling/ “pins and needles” pain

104
Q

What is Conn syndrome?

A

An adrenal adenoma (produces aldosterone–> primary hyperaldosteronism)

105
Q

Why might primary hyperaldosteronism result in patients having muscle weakness and paresthesias (tingling sensation)?

A

high aldosterone–> HTN (not hypernatremia bc of “aldosterone escape” with ANP to compensate for inc Na+ reabsorption), low K+ and H+ (pee out more)
With low K+ you can get muscle cramps and such.

106
Q

Patient has hyperpigmentation and ACTH stimulation test fails to stimulate cortisol production. What is a likely diagnosis?

A

Addison’s disease. (hyperpigmentation from inc ACTH which means inc MSH, or melanin stimulating hormone, too. And regardless of how much ACTH you give the patient, they are not able to produce cortisol- it’s low).
*Remember that Addison’s disease is adrenal insufficiency so the adrenal glands aren’t making any of their usual hormones well

107
Q

What does thyrotoxicosis mean?

A

An excess of thyroid hormone in the body.

108
Q

A 16 year old patient is brought in by her mom (who has hypOthyroidism) for concern of weight loss. She lost 10 lbs over the past 2 months but is not concerned about it herself–in fact, she still thinks she appears overweight. The girl also has high BP, HR, is anxious, and has increased reflexes. TSH is low, T4 is high, and Tg is not detectable. What’s probably going on?

A

She is taking her mom’s thyroid hormone pills to lose weight–> thyroidtoxicosis (too much thyroid hormone)
*note: we know the girl’s hyperthyroidism is NOT due to the thyroid gland making due too much TH because Tg is not detected. So, excess TH must be coming from an exogenous source.)

109
Q

A girl is taking thyroid hormone pills to lose weight. If a thyroid biopsy were taken, what would be seen?

A

Atrophy. Since the girl is taking exogenous thyroid pills, the thyroid gland will stop producing as much TH (negative feedback) and when organs are not used they atrophy.

110
Q

Most common cause of secondary hyperparathyroidism (inc PTH)?

A

chronic kidney disease

111
Q

Granulomas (like in TB) are formed from what type of T-cells?

A

CD4+

112
Q

Autosomal dominant mutations in what gene is the most common cause of familiar dilated cardiomyopathy (“I’m so tired” systolic dysfunction / pumping problem of the heart due to genetic cause)?

A

TTN gene (encodes for sarcomere protein titin)

113
Q

22 year old guy has palpitations and SOB. Suddenly collapses and dies. Autopsy shoes TTN gene and he had a family history of “early heart disease.” What did he have?

A

Familial dilated cardiomyopathy

“I’m so tired” systolic dysfunction / pumping problem of the heart due to genetic cause

114
Q

Treat DKA with insulin, fluid replacement, and potassium. Why K+?

A

DKA–> hyperkalemia (don’t have insulin to bring K+ into cells + metabolic acidosis means more H+ in blood that gets driven into cells and K+ driven out of cells into blood to balance charges). When you give the patient insulin, K+ will be driven into cells quickly–> hypokalemia. This is dangerous! So you give potassium to protect against hypokalemia.

115
Q

You take glucocorticoid steroids. What does that do to liver enzymes?

A

Increases them (talking about the liver enzymes that play a role in gluconeogenesis). Remember, steroids increase blood glucose (think of Cushing’s where you have inc Cortisol).

116
Q

Which anti-cholesterol medication can decrease renal excretion of uric acid—> gout?

A

Niacin

117
Q

Which congenital adrenal hyperplasia causes virilization and HTN in females?

A

11-OH deficiency.

118
Q

Patient has a type of Cushing’s syndrome. High-dose, but not lose-dose dexamethasone, suppresses cortisol levels. What’s the diagnosis?

A

Cushing’s disease (ACTH secreting pituitary adenoma).
Low-dose dexamethasone does NOT suppress cortisol levels—> means you give a low-dose steroid to the patient and cortisol made by the body does NOT goes down (when it should go down). This indicates a type of Cushing’s syndrome.
High-dose dexamethasone does suppress cortisol levels—> means you give a high-dose steroid to the patient and cortisol made by the body goes down (as it should). This indicates ACTH is being released by the pituitary gland and not some ectopic site like small cell carcinoma.

119
Q

You give a patient low-dose dexamethasone and it fails to suppress cortisol. What does this indicate?

A

Low-dose dexamethasone does NOT suppress cortisol levels—> means you give a low-dose steroid to the patient and cortisol made by the body does NOT goes down (when it should go down). This indicates a type of Cushing’s syndrome (increased production of Cortisol).

120
Q

You give a patient with a type of Cushing’s syndrome high-dose dexamethasone (to determine the type of Cushing’s syndrome they have) and it suppresses cortisol levels. What does this indicate?

A

Cushing’s disease.

High-dose dexamethasone does suppress cortisol levels—> means you give a high-dose steroid to the patient and cortisol made by the body goes down (as it should). This indicates ACTH is being released by the pituitary gland (Cushing’s disease) and not some ectopic site like small cell carcinoma.

121
Q

You give a patient with a type of Cushing’s syndrome high-dose dexamethasone (to determine the type of Cushing’s syndrome they have) and it FAILS to suppress cortisol levels. What does this indicate?

A

Ectopic ACTH secretion (for example, from small cell carcinoma).

High-dose dexamethasone does NOT suppress cortisol levels—> means you give a high-dose steroid to the patient and cortisol made by the body does NOT goes down (abnormal). This indicates ACTH is being released by some ectopic site like the lungs in small cell carcinoma (paraneoplastic syndrome)…cancer doesn’t care if you are pouring cortisol into the body. It’s a beast, so it will keep pumping out more cortisol anyway.

122
Q

Patient has DKA (for 2 days now). Bicarb is 14. CO2 is 40. What is going on: increased urinary bicarb loss or respiratory failure.

A

Respiratory failure.
Why? DKA= metabolic acidosis from acidic ketone bodies floating around. Since bicarb is low, the appropriate compensation would be hyperventilation (Kussumal breathing) to dec CO2 and this compensation should happen quickly! (Lung compensations are immediate- only kidneys take a while to compensate.) This patient is not breathing appropriately for DKA (breathing muscles wore out), so you can conclude it is respiratory failure. Plus the other option makes no sense- if you have low bicarb, why would the body react by peeing out more of its limited bicarb??

123
Q

Anti-tissue transglutaminase antibodies.

A

Celiac disease (gluten intolerance).

124
Q

Celiac disease can lead to malabsorption of what?

A

Dietary fats and fat-soluble vitamins (A, K, E, and D). (For example, celiac disease—> vitamin D deficiency).

125
Q

Patient has diabetes and a rash (necrolytic migratory erythema). What should you think of?

A

Glucagonoma (tumor of pancreatic alpha cells that secretes lots of glucagon).

126
Q

A patient is passed out in the grocery store from hypOglycemia. What can you do to help?

A

Give the patient intramuscular glucagon (glucagon will stimulate gluconeogenesis and glycogenogenesis in the liver to make more glucose).
Note: you can’t just hand the patient some orange juice to drink bc she is passed out! This is the solution for more mild hyperglycemia when the patient is conscious.

127
Q

In familial hypocalciuric hypercalcemia, are calcium levels high or low? How about PTH levels? Explain it.

A

Familial hypocalciuric hypercalcemia- you have defective calcium-sensing receptors so you have to have a crazy ton of calcium in the blood to stimulate them to lower PTH (and consequently lower calcium). So, calcium and PTH are high in this condition.

128
Q

What lipid-lowering agent will do the best job of lowering TAGs?

A

Fibrates

129
Q

Alcoholic with epigastric pain and elevated TAGs. What should you think of?

A

Pancreatitis

130
Q

Which T2DM drug class is most linked to hypoglycemia as a side effect?

A

Sulfonyureas (1st gen- chlorpropamide, tolbutamide, 2nd gen- glimepride, glipizide, glyburide)

131
Q

Glucocorticoid steroids decrease immune cells, except they increase what type of immune cell?

A

Neutrophils (why? Bc they cause neutrophils sticking on the vascular wall to detach and circulate in the bloodstream—> inc neutrophil count)

132
Q

Hypoglycemia guy is injected with glucagon and recovers. What organ underwent changes leading to the recovery?

A

The liver.

Glucagon—> gluconeogenesis (making of glucose) in the liver

133
Q

What drug can be given to men with gynecomastia (breast enlargement)?

A

Tamoxifen (antagonist at the breast)

134
Q

A person has been exposed to radioactive 131 iodine. What can be given to protect their thyroid?

A

Potassium iodine

135
Q

Before you start a T2 diabetic patient on Metformin, what should you check?

A

Their serum creatinine (make sure they do not have renal insufficiency- if they do, use Metformin with caution, as it can cause lactic acidosis as a side effect!)

136
Q

What types of insulin are usually given to diabetics?

A

Long-acting (or intermediate acting) to establish baseline all day + short-acting to take before meals.

137
Q

What are the rapid-acting insulin preparations?

A

Glulisine, Aspart, and Lispro

“Girls And Lads” in Sketchy

138
Q

What are the long-acting insulin preparations?

A

Detemir and Glargine

“Don’t Go” in Sketchy

139
Q

What are the intermediate-acting insulin preparations?

A 
Regular insulin (can also be classified as short-acting) and NPH
(“Rest Now” in Sketchy)
140
Q

What is the mechanism of Anastrozole, Exemestane, and Letrozole in helping with estrogen receptor- positive breast tumors?

A

These meds block the conversion of androgens to estrogen by blocking the enzyme Aromatase. Decreasing estrogen production helps with control of an estrogen receptor positive tumor.

141
Q

What kind of cell junctions are involved with labor contractions in the uterus/ cervix? What proteins make up these cell junctions?

A

Gap junctions- made of connections (proteins that assemble into gap junctions. These increase with increasing estrogen levels.)

Gap junctions are for communication and coordination between cells, which is needed for labor contractions.

142
Q

What does nulliparity mean?

A

The woman has never given birth.

143
Q

What does “cervical abnormalities” refer to?

A

Cervical dysplasia, usually from HPV (HPV 16, 18, 31, or 33–> CIN (dysplasia)—> squamous cell carcinoma of the cervix)

144
Q

What is the basal cell layer?

A

The innermost layer of the epithelial cells

145
Q

What are caspases?

A

Proteolytic enzymes that destroy cell components (involved in apoptosis)

146
Q

Apical holosystolic murmur. What is it?

A

Mitral regurgitation (the apical region of the heart= mitral valve and systolic means it must be mitral regurgitation, or problem with valve closure, bc the mitral valve closes in systole)

147
Q

What will help make mitral regurgitation better: dec HR, dec SVR/ afterload, dec preload, inc contractility, or inc preload?

A

Decreasing afterload.
Why? Blood will take the path of least resistance. If there’s lower pressure in the RA than in the pulmonic arteries, that promotes back flow in a regurgitant valve (problems closing). However, if afterload (the pressure of forward flow) is lowered, more blood will take that and less blood will regurg.

148
Q

Would you expect decreased or increased values for the following in a COPD patient? FEV1, TLC, and diffusion capacity

A

FEV1 decreased
TLC increased
Diffusion capacity decreased

149
Q

How does Diphtheria kill host cells?

A

It’s exotoxin (A:B) inhibits protein synthesis by ribosylation of elongation factor 2 (EF-2)—> cell death—> formation of psuedomembranes (grayish exudates in the throat)

150
Q

What is babesia? (Bacteria, virus, parasite, fungi)

A

Parasite

151
Q

What kind of bug causes Babesiosis?

A

The Ixodes tick

152
Q

What can Babesia (from Ixodes tick) do to the blood?

A

Cause hemolytic anemia (shistocytes)

153
Q

What does pleocytosis mean?

A

Increased cells (usually inc WBCs in CSF)

154
Q

What vulvar lesions would be seen in primary, secondary, and tertiary syphilis?

A

Primary—> chancre (painLESS lesions)
Secondary—> condyloma lata (wart-like growths that disseminate/ spread with rash on body too)
Tertiary—> gumma (necrotizing granulomas that occur with cardiac issues like aortic tree-barking/ murmur and other nasty systemic symptoms)

155
Q

What’s the difference between condyloma latte and acumita?

A

Both warts

HPV—> condyloma acumita (warts)

Syphilis—> condyloma latte (flat warts)

156
Q

Neurosyphilus can occur in what stage of syphilis?

A

Any! Primary, secondary, or tertiary

157
Q

MHC I and II are found on what cell types?

A

MHC II on APCs (antigen-presenting cells)

MHC I on all cell types

158
Q

How can alcoholism lead to coagulation problems?

A

Alcohol destroys the liver and the liver makes coagulation factors.

159
Q

Which clotting factors are activated by vitamin K?

A

Factors 2, 7, 9, 10, protein C, and protein S

Made by the liver, activated by vitamin K

160
Q

Increased prothrombin time (PT) and giving K+ doesn’t help. What does this indicate?

A

Factor 7 deficiency

(PT goes along with the extrinsic pathway, which involves factor 7 only. Factor 7 is one of the ones vitamin K activates— vitamin K activates 2, 7, 9, 10, protein C and S— so could be a vitamin K deficiency. But we gave the patient vitamin K and it didn’t help so it’s not. Must be a factor 7 deficiency.)

161
Q

What kind of DNA is circular and codes for proteins, tRNA, and rRNA in eukaryotic cells?

A

Mitochondrial RNA

162
Q

Why give nitrates to angina patients?

A

Primarily venodilate (also vasodilate). This decreases preload to heart—> decreases work of heart.

163
Q

Stress incontinence is caused by weakened pelvic floor muscles called what (anatomy)?

A

Levator Ani muscles

164
Q

Lady from an endemic country with a dog has eggshell calcifications in liver and hepatomegaly. Dies after surgery. What was she infected with?

A

Echinococcus Granulosus (tapeworm transmitted by dogs and sheep—> cyst formation in liver—> rupture of cysts leads to anaphylactic shock)

165
Q

Where does transcription start? Where does translation start? (The codon)

A

Transcription starts at the “TATA box.” Translation starts at AUG (ends at UAA, UGA, UAG- “you are annoying, you go away, you are gone”)

166
Q

What factors are needed to grow H.flu on culture? Why does growing it with staph A. Help?

A

Needs factor X (10) aka hematin and factor V (5) aka NAD+. Staph A can promote its growth bc it provides these factors.

167
Q

What’s the single most important measure to reduce risk of hospital-acquired infections (such as MRSA)?

A

Hand hygiene (note that isolation is only necessary for airborne infection like TB)

168
Q

What 3 cytokines are critical for the formation and maintenance of granulomas (such as in TB)?

A

IL-12, IFN-gamma, and TNF-alpha

169
Q

60 year old guy. Smoker. Blood in urine. Hypercalcemia and erthyrocytosis (inc RBCs). CT shows something going on with the kidneys. What is it?

A

RCC (renal cell carcinoma)
*Most commonly occurs in men 50-70 years old. Smokers at inc risk. Manifests as hematuria. Associated with paraneoplastic syndromes, such as PTHrP—> hypercalcemia and ectopic EPO—> inc RBCs.

170
Q

Why can a person get re-infected with Gonorrhea (even though antibodies form once exposed the first time)?

A 
Antigenic variation (can modify their pilli protein)
*this is also why we haven’t made a vaccine against Gonorrhea (or the common cold...)
171
Q

What bacterial factor is responsible for E. Coli that causes gram negative sepsis?

A

LPS (lipid A is the toxic/ active component)

172
Q

What valve is most commonly involved in bacterial endocarditis (by staph a., strep viridans, etc.)?

A

Mitral valve

173
Q

A guy has gradual onset SOB, non-productive cough, fatigue. Chest x-ray shows restrictive pattern. History of rheumatoid arthritis, has been taking meds for a long time. What is it?

A

Pulmonary fibrosis

*may see “honeycomb” lung appearance

174
Q

What is negative predictive value?

A

Test result comes back negative—> the probability it’s correct and you actually do NOT have the disease

175
Q

Most common cause of death in a Marfan’s syndrome patient?

A

Aortic dissection

176
Q

The influenza vaccine is what type of vaccine? How does it work?

A

Killed vaccine. Creates a humoral response against extracellular viral antigens (killed virus gets loaded onto MHC II—> interacts with CD4+ T-cells). Inhibits viral entry into cells.

177
Q

Explain hyperactive transplant rejection.

A

Rejection to a transplanted organs WITHIN MINUTES. The recipient’s body happened to have already had antibodies floating around that recognized foreign protein of the transplant organ as soon as you put it in. So the new organ dies (ischemia/ necrosis) just as you put it in and it must be taken out.

178
Q

What serotype of Chlamydia causes painful, inflammed inguinal lymph nodes that ulcerate into buboes (known as lymphogranuloma venereum)?

A

L1-L3

179
Q

What serotype of Chlamydia is the STD (most common STD in the US)?

A

D-K

180
Q

What serotypes of Chlamydia cause blindness?

A

A-C

181
Q

“Reticulocytes that replicate intracellularly” is a buzzword for what?

A

Chlamydia

184
Q

What is almost a requirement in order for UTIs to turn into kidney infections (pyelonephritis)?

A

Vesicoureteral reflex (when urine from the bladder reflexes back the wrong direction through the ureters toward the kidneys)

185
Q

What are the “4 C’s” to diagnose measles?

A

Cough
Coryza (runny nose)
Conjunctivitis
Koplix spots (errythemia on the buccal mucosa)

186
Q

What vitamin do you give to measles patients to decrease morbidity and mortality?

A

Vitamin A

187
Q

Congenital microcephaly is associated with what virus?

A

(Microcephaly= small head)

Zika virus

188
Q

HAART (anti-retroviral) therapy has what affect on fat as a side effect?

A

Body fat redistribution

189
Q

Guy who recently had an MI is taking a drug that led to him now having elevated serum creatinase. What drug?

A

A statin (causes breakdown of muscle—> myopathy as a side effect), given to CAD patients

190
Q

Holosystolic murmur at the apex with radiation to the axilla is what?

A

Mitral regurgitation

191
Q

Explain why you hear an S3 gallop in mitral regurgitation.

A

Mitral regurgitation means the mitral valve is having a hard time closing and blood is flowing back from the left ventricle (LV) to the left atrium (LA). Now there’s extra blood in the LA that will fill the LV at diastole. Extra blood into a ventricle (blood going into already overfilled ventricle)= S3.

192
Q

When is the S4 heart sound?

A

Blood colliding into a stiff ventricle (occurs during atrial kick of ventricular diastole).

193
Q

If there is no S3 heart sound, can there be mitral regurgitation?

A

No. Mitral regurgitation will always produce an S3 heart sound from blood going into an already overfilled ventricle (blood flows back from LV—> LA so there will be extra blood filling up the LV at the next diastole)

194
Q

65 year old male, smoker, has HTN. There’s a pulsating central abdominal mass on physical exam. What is it?

A

Abdominal aortic aneurysm

due to atherosclerosis, inflammation—> fibrosis and weakening of the arterial wall

195
Q

What are the 3 encapsulated bacteria that asplenic patients are more prone to getting?

A
  1. Strep Pneumo
  2. H. Flu
  3. N. Meningitis
196
Q

Guy gets into a car accident and requires emergency surgery to deal with internal bleeding. What organ most likely ruptured?

A

The spleen

197
Q

Sickle cell and asplenic patients are more prone to getting what type of bacterial infections? Name the specific ones.

A

Encapsulated bacteria.

  1. Strep Pneumo
  2. H. Flu
  3. N. Meningitis
198
Q

Is cholelithiasis more or less common during pregnancy?

A

Cholelithiasis= gallstones. More common in pregnancy (and on oral contraceptives) due to inc levels of estrogen (inc cholesterol secretion) and PG (relaxation of the gallbladder)

199
Q

Why pregnant women and women on OCP’s more prone to getting gallstones?

A

High levels of estrogen—> inc secretion of cholesterol

High levels of progesterone (PG)—> gallbladder hypOmotility
(Remember, PG is “pro-gestation” and systemically is a smooth muscle relaxant to keep the baby in- you need the uterus to be relaxed not contracting to maintain pregnancy. It has the same effect on the gallbladder, that is, relaxation and not contraction.)

200
Q

How can carotid massage help a patient with paroxysmal supraventricular tachycardia (PSVT)?

A

It decreases heart rate.

Carotid massage (apply pressure to carotid arteries)—> inc stretch—> more afferent baroreceptor firing—> inc AV node refractory period—> dec HR

Note that carotid massage will cause the parasympathetic (rest and digest) response to kick in which means dec BP (this is why doing bilateral carotid massage to an elderly patient can cause them to pass out) AND dec HR.

201
Q

ANP and BNP act via what cell signaling cascade?

A

Increased cGMP

202
Q

What is alternative splicing?

A

Process by which a single gene can code for various unique proteins by selectively including or excluding different DNA coding regions (Exxon’s) into mature mRNA

203
Q

What ions are lost in vomiting? Diarrhea?

A

Vomiting—> lose H+, Cl-, K+

Diarrhea—> lose HCO3- (bicarb), K+

204
Q

Is vomiting metabolic acidosis or alkalosis? How about diarrhea?

A

Vomiting—> lose H+, Cl-, K+
This is a metabolic ALKALOSIS (lose H+—> parietal cells in stomach will make more HCl acid to compensate—> as H+ is made to be secreted into the stomach, HCO3- is also made and pushed into the blood, called “alkaline tide” on FA page 392. Inc HCO3- = metabolic alkalosis.)

Diarrhea—> lose HCO3- (bicarb), K+
This is a metabolic ACIDOSIS (dec HCO3- = metabolic acidosis)

205
Q

What is normal body temperature? What is a fever defined as clinically?

A

Normal body temp= 98.6 degrees

Fever= 100.4 degrees or higher

206
Q

You suspect child abuse. What do you do first: try to interview the child alone or contact CPS?

A

Try to interview the child alone (then contact CPS)

207
Q

Do positive and negative predictive value depend on disease prevalence? How about specificity and sensitive?

A

Positive/ negative predictive value DO depend on disease prevalence. If a disease is more common, there’s a higher positive predictive value (if you get a positive test result, it’s more likely to be true/ true positive).

Specificity and sensitivity do NOT depend on disease prevalence.

208
Q

Why is hep C genetically unstable (has variation)?

A

Vision exonculease lacks proofreading capacity in 3’—> 5’ direction so it is prone to mutation

(Remember the Hep C and hippos in Sketchy with sign “no viewing from 3-5”)

209
Q

What is small bowel syndrome?

A

Massive bowel resection or Crohn’s disease (where there are skip lesions and parts of the bowel that are inflamed and not working)—> decreased intestinal surface area and transit time—> diarrhea and weight loss from malabsorption
(If there is loss of function in the terminal ileum, which is the most common site Crohn’s affects, you’d get vit B12 deficiency)

210
Q

What is the first thing that initiates appendicitis?

A

Obstruction of the lumen of the appendix.
This obstruction can be a fecalith, tumor, lymphoid aggregate…
(Note: bacterial infection can occur and play an important role in appendicitis, but this is not the first event that triggers it! You get obstruction to the appendix lumen—> inflammation)

211
Q

Patient has bloody diarrhea from E. Coli. What type of E. Coli is this? What is the mechanism of its toxin?

A

EHEC (remember H for hamburger—> bloody diarrhea. Vs. ETEC remember T for traveler—> watery diarrhea) (specifically strain 0157:H7)
Shiga-like toxin that inhibits the 60s ribosomal subunit

212
Q

Guy has colon cancer (adenocarcinoma), no polyps found. He has a family history of colon CA and endometrial CA. What does he probably have?

A

Lynch syndrome aka hereditary nonpolyposis colorectal cancer (HNPCC)
(Autosomal dominant mutation in DNA mismatch repair genes MSH2, MLH1, MSH6, or PMS 2–> Micro-satellite instability (MSI)—> colon cancer, no pre-cancer polyps first)

213
Q

Man has blood on toilet paper when he wipes. Pain with defecation. History of constipation. What is going on?

A 
Anal fissure
(Note: this presentation is also like external hemorrhoids below the pectinate/ dentate line, but the fact that he has constipation and straining a lot makes anal fissure, or tearing in anal mucosa below the pectinate/ dentate line, more likely)
214
Q

What is an anal fissure, where does it occur? What things can lead to this?

A

Tear in anal mucosa below the pectinate/ dentate line.
“Pectinate line. Pain while pooping. Blood on tP. Located Posteriorly bc this area is Poorly Perfused”
Things that can lead to this: constiplation (straining), frequent diarrhea, anal sex (note there is poor perfusion in the posterior anal canal, which makes its mucosa sensitive to trauma and slows healing times)

215
Q

Lynch syndrome is associated with what types of cancer?

A

Endometrial, ovarian, and skin CA

(Remember, Lynch syndrome aka hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant mutation in DNA mismatch repair genes—> microsatellite instability (MSI)—> colon CA w/o pre-cancer polyps first)

216
Q

How might an alcoholic get splenomegaly?

A

Alcoholic liver damage—> Portal hypertension—> blood backs up to spleen (portal vein—> splenic vein)

*note: the part of the spleen that would be enlarged is the red pulp (where RBCs/ blood are)

217
Q

What hormone can decrease portal venous pressure in a patient?

A

Somatostatin (or Octreotide, a somatostatin analog)

Remember “somato-STOP-in”
Helps with variceal bleeding

218
Q

Lady has CAD, SOB, elevated JVP. Hepatomegaly. Liver biopsy shows central necrosis- why?

A

She has right heart failure—> blood backs up through IVC—> hepatic vein—> central veins (reason the necrosis in the liver is centralobular aka in the middle of the lobules where the blood flows through). This is congestive hepatopathy.
(Basically, right sided HF—> back up of blood in the liver—> big liver)

219
Q

A patient has FAP(familial adenomatous polyposis), so she has an APC mutation. What is the likelihood she will develop colon CA?

A

100%. Remove the colon prophylactically (prevent colon CA progression).

Block 8 (3 decks)

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