Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

USLME Kiss my ass and pray > endo DIT > Flashcards

endo DIT Flashcards

1
Q

cAMP modifying hormones (11)

A 
FSH
LH
TSH
hCG
ACTH
MSH
GHRH
PTH
Calcitonin
glucagon
V2 vassopressin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IP3 modifying hormones(4)

A

GNRH
TRH
Oxytocin
vasopressin (v1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tyrosine kinase receptor modulators

A 
GH
Insulin
insulin like growth factor
Platelet derived growth factor
fibroblast growth factor
Cytokines
prolactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cGMP modulators (2)

A

NO
ANP

the vasodialators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Preganancy leads to an increase of what liver product that may affect hormone affects

A

binding globulin decreasing the amount of free active hormone

Thyroid - TGH for example

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Steroid receptor modulated hormone (5)

A 
estrogen, progesteron, testosterone
glucocorticoids
aldosterone
Thyroid hormone
Vit D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Availabilty of binding hormone affects 2 things

A

amount of free hormone

activity of steroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

increased sex binding hormone may have what affect on men?

A

gynectomastia due to decreased free testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

decreased sex binding hormone in women may have what effect in women?

A

hurtusism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ACTH and MSH are synthesized by what precursor?

Clinical relevance?

A

POMC

Leads to hyperpigmentation w/ primary adrenal insufficency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hyperprolactenima due to? (4)

A

pregnancy/ nipple stim
stress
prolactinoma
dopamine antagonists ) haloperidol, risperidone, domperidone, metoclopramide, methydopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Symptoms of hyperprolactinemia in

pre meno women

post meno?

Men

A

hypogonadism -> infertility, oligo/amennorhea, rarely galatorrhea

post meno - asymptomatic, maybe galactorrea

Men - (low testosterone)low labido, impotence, infertility, gynectomastia, rarely galactorrhea

remember, prolactin inhibits FSH and LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical uses of octreotide(3)

A

pituitary excess
-acromegaly, thyrotropinoma, ACTH secreting hormones

GI endocrine excess
-Zollinger ellison syndrome, carcinoid, VIPoma, glucagona, insulinoma

Need to reduce splanchnic circulation
-portal HTN, bleeding peptic ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

infertility, galactorrhea and bitemporal hemanopsia

A

prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

inability to breastfeed, amenorrhea, cold intolerance

A

sheehan syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which hormones share a common alpha subunit(4)

A

TSH
LH
FSH
b hCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

anterior pituitary is derived from

A

rathke’s pouch

surface ectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

posterior pituitary is derived from

A

neuroectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ADH is stimulated w/ ?(3)

Decreased w?(3)

A

nicotine
opiates
high serum osmolarity
low volume contraction

ethanol
atrial naturetic factor
low serum osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Oxytocin important w/

stimulated w?

A

pregnancy and breast feeding
uterine contraction ( return to normal size/clamp bleeding)
milk ejection

cervical dilation
inhibited w/ alcohol and stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

inhibit feeds back and blocks

A

FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

progesterone and testosterone feedback on

A

LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ACTH is stimulated to release w/(2)

A

Stress

CRH from the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TSH is released from?

inhibited by?

Stimulated by?

A

TSH from the pituitary

inhibited by T3 and T4 levels

Stimulated by TRH from hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Prolactin leads to inhibition of ?

Prolactin stimulated by?

A

ovulation via blocking of LH and FSH
- stimulates milk production and breast development

stimulated to release by TRH and less Dopamine inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

GH effects (4)

A

increases growth
decreases glucose uptake (insulin resistent- mobilize gluc)
increase protein synth
increase organ size and lean body mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

upstream control of GH (2)

other regulators of release(environmental)

A

GHRH - releases
GHIH (somatostatin)

+: exercise, sleep, hypoglycemia, puberty, estrogen, stress, endogenous opiods

-: obesity, hyperglycemia, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Downstream response to increase of GH

A

increase of IGF 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Rx for prolactinoma

A

dopamine agonists

  • bromocriptine
  • cabergoline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Presentation of Acromegaly

A 
large tounge
deep voice
large hands/feet
coarse facial feature
impaired glucose tolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Diagnosis of acromegaly (2)

A

measure IGF1 - more stable vs pulsitile GH

failure of suppression of GH from the pituitary adenoma w/ glucose given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Zona glomerulosa secretes

responds to

A

Aldosterone

renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Zona fasiculata secretes?

responds to

A

cortisol

ACTH and CRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Zona reticularis secretes?

Responds to?

A

androgens

ACTH and CRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Adrenal tumor in adult vs kids

One key difference

A

Pheochromocytoma in adults -> episodic periods of hypertension

Neuroblastoma in kids -> maybe chronic HTN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Symptoms of a pheochromocytoma (4)

A

HA, Sweats, Tachy, Eposodic HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fetal adrenal gland is important in

A

secretion of cortisol for fetal lung maturation

responds to CRH and ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ketoconazole acts to block what enzyme?

A

desmolase

-conversion of cholesterol -> pregnenolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

ACTH acts on what enzyme to encourage hormone synthesis?

A

Desmolase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Angitension II acts on adrenal steroid synthesis by increasing the action of what enzyme

A

aldoserone synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

One thing in common w/ adrenal hyperplasia

A

all have decrease production of cortisol

  • > ACTH ramps up
  • > stimualtes adrenal cortex
  • > adrenal hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Enzyme responsible for converting testosterone to a more active enzyme

Blocked by what drug

A

5 alpha reductase

blocked by finasteride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

estone, estradiol and estriol all need what enzyme to be made?

A

Aromatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Features of 3 beta hydroxysteriod deficiency? (3)

A

Inability to produce

  • glucocorticoids
  • mineralcorticoids
  • androstenedione-> testosterone or estrone
  • estrogens

Excessive Na excretion in the urine (salt wasting)

Early death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What features are characteristic in 17 alpha hydroxylase deficiency

A

inability to produce androgens/sex hormones and cortisol
-> phenotypic female that is unable to mature (no androstendione)

Hypertension w/ everything being shunted to aldosterone production
-Na and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Desmolase is responsible for what

A

converting cholesterol to pregnenolone starting the adrenal steroid pathway

rate limiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What features are characteristic of a deficiency in 21 alpha hydroxylase? (3)

A

Can’t make cortisol or aldosterone ->

Increased ACTH

Hypotension and salt wasting w/ou Aldosterone

Masculinization w/ everything shunted to the right (androstenedione)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What features are characteristic of 11 beta hydroxylase deficiency?

A

Inability to produce Aldosterone and Cortisol

Increased ACTH

Increased production of 11 deoxycorticosterone
-Acts as a weak aldosterone -> HTN

masculinization with a shift to sex hormone production (androstenedione)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

2 deficiencies characteristic in hypertension

A

11 beta hydroxylase

17 alpha hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

2 deficiencies characteristic in masculinization

A

21 hydroxylase

11 beta hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

deficiency characteristic in hypotension

masculinization of feminization

A

21 hydroxylase

masculinization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Cortisol maintains BP how?

A

increasing alpha 1 receptors on the vasculature increasing sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Cortisol functions/effects on the body (5)

A

BBIG

Maintain BP increasing alpha receptors on vasculature

Decreases bone formation

Anti inflam/immune suppresive
-neutropenia w/ adhesion disruption, inhibits prostaglandin production, block IL2

Insulin resistance (diabetogenic)

Gluconeogenesis/lipolysis and proteolysis ( increases enzyme expression)-> mobilizes sugars

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Why is there a rise in WBC after giving a glucocorticoid

A

neutropenia transient due to mobilization of WBC stores in the vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Regulation of cortisol 3 steps

A

CRH from the hypothalamus

  • > Pituitary releasing ACTH
  • > ACTH acts on the adrenal cortex (desmolase) to increase production of cortisol in the zona fasiculata
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What can induce prolonged secretion of cortisol

A

chronic stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Symptoms of Cushing Syndrome

A

BAM CUSHINGOID

Buffalo hump
Amenorrhea
Moon Fascies

Crazy 
Ulcers (peptic)
Skin ∆s (striae, acne)
HTN
Infection
Necrosis of femoral head
glaucoma.cataracts
Osteroperosis
Immunosuppression
DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

4 Causes of Cushing Syndrome

A

Iatrogenic (exogenous steriods - #1)
Pituitary Adenoma - Cushings disease (ACTH)
Ectopic ACTH production - small cell
Adrenal adenoma (primary high cortisol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Dexamethasone suppression test w/ high dose will suppress cortisol of which cause of cushing syndrome?

A

Suppreses pituitary adenoma

ACTH levels to differentiate between adrenal adenoma and small cell - both unsuppresed

  • high ACTH in ectopic (small cell)
  • low ACTH in adrenal adenoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Presentation of HTN, hypokalemia and metabolic alkalosis due to

A

Conn Syndrome
- Primary hyperaldosteronism

Have a low renin level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

primary hyperaldosteronism name?

Triad of symptoms

A

Conn syndrome

See:

  • Hypertension
  • Hypokalemia
  • metabolic alkalosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Rx for Conn syndrome (2)

A

epleronone and spironolactone

Surgery

prevent hyperaldosertone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Secondary hyperaldosteronism due to: (4)

A

renal artery stenosis

chronic renal failure

CHF

hypo protein states (edema perceived fluid loss)

  • cirrosis
  • nephrotic syndrome

Going to have high renin levels (appropriately)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Fludrocortizone

A

highly active synthetic mineral corticoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Stimulation of Aldosterone

decreased aldosterone secretion

A

Decreased
-high Na

Increased in

  • low Na or volume
  • Hyperkalemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Addisons is most commonly due to

Presentation

A

autoimmune attack of the adrenal cortex -> chronic primary adrenal insufficiency ( less aldosterone, cortisol)
–Less commonly: TB and METs

low aldosterone and cortisol ->

  • hypotension
  • skin pigmentation
  • hyperkalemia
  • acidosis
  • malaise
  • anorexia
  • fatigue
  • weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Primary adrenal insufficiency can be distinguished from secondary adrenal insufficiency by :

A

Increased amount of ACTH in primary adrenal insufficiency

Decreased in secondary adrenal insufficiency (problem is in the pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Secondary adrenal insufficiency presents as?

Due to

A

less ACTH due disruption of the pituitary ->

malaise
fatigue
weight loss
anorexia

NO skin pigmentation (no POMC)
NO hyperkalemia/hypotension (Aldosterone from renin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How do you have hypotension w/ Addison’s

A

chronic primary adrenal insufficiency

no alpha 1 upregulation w/ cortisol
No aldosterone leading to water and Na retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Cause of acute adrenal insufficiency

A

adrenal hemorrhage w/ Nessieria meningitidia
(waterhouse frederichsen syndrome

  • Septic
  • DIC
    endotoxic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Urine product detecting pheo?

Serum product looking for a pheo?

A

VMA ( vanilla mandelin acid) in urine

Normetanephrine and metanephrine in serum

catecholamine breakdown products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Pheos can be associated w which 3 tumor syndromes

A

MEN 2A
MEN 2B
neurofibromatosis 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Erythropoeitin can be secreted in 4 tumors

A

Pheochromocytoma
Renal cell carcinoma
hemangioblastoma
hepatocellular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Medical treatment for a pheochromocytoma?(3 steps

A

1st manage the BP w/ alpha 1 antagonist - phenoxybenzamine

  1. maybe give a beta blocker
  2. surgically remove the chromatin cell/adrenal medulla cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Rule of 10s w/ a pheochromocytoma (5)

A 
90% benign
90% adults
90% adrenal - occasionally extra renal
90% do not calcify
90% unilateral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

most common tumor of the adrenal medulla in kids

presentation/location?

test for urine?

A

neuroblastoma

tumor can be anywhere in the sympathetic chain 40% adrenal

less likely episodic HTN

homovanillic acid (dopamine breakdown) in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

neuroblastoma is associated w. over expression of this oncgene

Histological stain to help differentiate

A

n-myc

can stain for neurofilaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Bombeison tumor marker associated w?

A

neuroblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

MEN 1 tumors

associated mutation

A

mutation in p53

3 Ps

Pituitary adenoma
Parathyroid adenoma**
Pancreatic tumors (VIPoma, gastrinoma, insulinoma, zollinger ellison, glucagonomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

MEN 2a tumors

associated mutation

A

mutation in ret gene

PP’s and M

Medullary thyroid carcinoma* (secretes calcitonin)
Pheochromocytoma
Parathyroroid tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

MEN 2 B tumors

associated mutation

A

mutation in ret gene

1P and 2 Ms

Medullary Thyroid Carcinoma
Pheochromocytoma
Mucosal neuromas (ganlioneuromatosis of the Gi and oral cavity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

MEN syndrome inheritence

A

all auto recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

presentation of kidney stones or stomach ulcers w/ weigh loss

be concerned of what?

A

MEN 1

  • parathyroid tumor -> PTH -> excess Ca
  • Pancreatic tumor -> gastrinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

most common cause of Conn syndrome

A

adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Thyroid is derived from what tissue in what location?

A

ectoderm
originates from the floor of the primitive and descends into the neck via the thyroglossal duct

foramen cecum is site of origination and most common site of ectopic thyroid tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

anterior midline mass that moves with swallowing is what?

Derived from

A

thyroglossal duct cyst that is due to persistent thyroglossal duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Function of T3 and T4

A

ramps up metabolism
- bone growth (synergy w/ GH)
-CNS maturation
increase in beta 1 receptors of the heart
increased basal metabolic rate via increased Na/K atpase activity
increased glycogenolysis, gluconeogenesis. lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Thyroxine binding globulin increased w?

Decreased w?

resulting lab values

A

Increased TBG in pregnancy and OCP use

  • leads to increase in total T4 and T3 w/ binding of free hormone
  • percieved depletion of free hormone leads to increase in release which is again bound up -> normal/elevated T3/T4

TSH can be low due to similarity to beta hCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Enzyme responsible for oxidation and organification go iodide?

A

Peroxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Iodide is brought into the follicular cell via?

Bound to what AA residue

A

Na/I cotransporter

then oxidized to Iodine and bound tyrosine AA residue on thyroglobulin (organification)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

2 drugs to prevent thyroid hormone synthesis

Which is preferred overall?

Which is preferred in pregnancy

A

propylthirouracil

  • blocks peripheral conversion of T4-> T3
  • used in 1st trimester
  • generally worse SFx profile w/ agranulocytosis, liver dysfunction

methimazole

  • preferred over all
  • used in 2nd and 3rd trimester only due to risk aplastic cutis in 1st
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Symptoms of hyperthyroidism

A 
heat intolerance -> due to production/metabolism
weight loss
hyperactivity
diarrhea
increased reflexes
pretibibial myxedema - graves
warm moist skin
tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Lab value used to screen for hyperthyroidism

A

TSH would be low

-very responsive to small changes in T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

brief episode of hyperthyroidism followed hypothyroidism, painful thyroid on palpitation?

entire episode was preceded by what event?

A

subacute thryroiditis

Usually preceded by a viral/ flue like illness

95
Q

Rx for subacute thyroiditis?

see on histology?

A

NSAIDs for pain for it is usually self limiting

granulomatous inflammation

96
Q

HLA B35 assoicated w/ this thyroid pathology

see on histology

A

subacute thyroiditis

granulomatous inflammation

97
Q

Focal patches of hyper functioning follicular cells working independently of TSH due to mutation in TSH receptor

Reassurance on radioactive iodide uptake?

A

toxic multinodular goiter

increase release of T3 and T4 seen

Look for HOT nodules -> rarely malignant

98
Q

Jod Basedow phenomenon

A

patients beocmes thyrotoxicosis after being given exogenous iodine (post CT w/ contrast or amiodarone) and patient has a thyroid deficiency goiter and goes crazy w/ now iodine

99
Q

Graves disease presents as?

Due to

A

presents w/ hyperthyroidism, pretibial myxedema and exothalamos due to presence of TSH receptor location; and a diffuse goiter

due to autoimmune creation of thyroid STIMULATING (odd) immunoglobins (IgG) that act as TSH -> increase of T3 and T4 release

100
Q

HLA DR3 and HLA B* are associated w/ what thyroid pathology

101
Q

Thyroid storm is due to?

Rx?

A

stress induced catecholamine surge leading to death by arrhythmia ( restless, fever, sweating, tachy, tremor, delirium, vomiting, change in mental status)

Complication of graves and other hyperthyroid disorders

Rx: beta blockers, propylthiouricil, methimazole

102
Q

stroma ovarri teratoma

A

teratoma w/ functional thyroid tissue -> hyperthyroid presentation

RARE

103
Q

recent injection using a IV contrast leads to presentation of hyperthyroidism

A

Jod Basedow

104
Q

presents as hyperthyroidism post thyroidectomy or radio ablation of thyroid

A

given too much T3 and T4

105
Q

graves disease TSH and T3/T4 levels

A

TSH is low, Thyrois stimulating immunoglobin (IgG) acting on thyroid ->

High T3/T4

106
Q

Body mostly makes what type of thyroid hormone

A

T4

Stable 6-9 days. longer half life

107
Q

histology of 3 main hypothyroid states

hashimotos
subacute thyroditis
Riedals

A

Hashimotos
-lymphocyte infiltration, Hurthel cells

Subacute
-granulomatous infiltration

Reidal
-fibrous w/ macrophage and eosinophil infiltration

108
Q

Most common cause of hypothyroidism

See what in serum potentially?

A

hashimotos

thyroid peroxidase antibodies
antithyroglobulin antibodies

109
Q

increase risk of what CA w/ hashimotos?

Commonly associated w?

A

B cell lymphoma

other autoimmune pathologies: Addisons, DM, sjogrens

110
Q

Transient hyperthyroid for a couple months, painless thyroid, eventually hypothyroid

A

hashimotos

111
Q

HLA DR5 and HLA B5 are associated w?

A

Hashimotos

112
Q

Causes of congenital hypothyroidism(5)

A

Cretism

defect in T4 formation
developmental failure
failure of descent
iodine deficient mother (most common world wide)
transfer of mother’s auto-ab/medication across placenta

113
Q

Presentation of congenital hypothyroidism (4)

A

Pot bellied
mental retardation
protuberant tongue
dwarfism (lack of synergy w/GH)

114
Q

Reidals thryroiditis presentation

A

thyroid replaced w/ fibrous tissue (fixed/ rock hard/ painless goiter)

concern w/ extension into local tissue and compression

Histology you see eosinophilia and macrophage infiltration

115
Q

fixed, hard painless goiter

116
Q

levothyroxine

A

synthetic T4

usually what is given once a day for hypothyroidism

117
Q

Triiodothyronine

A

synthetic T3

not used as much as levothyroxine

118
Q

Presentation of hypothyroidism

A 
cold intolerance
weight gain
hypoactivity/lethargy
constipation
decreased reflexes
dry cool skin/brittle hair
bradycardia
119
Q

hypothyroidism has what effect on lipid profile

A

increases LDL and total cholesterol

120
Q

Papillary carcinoma prevelance and presentation (4)

A

most common

empty appearing nuclei/orphan annie/ ground glass
psammoma bodies
nuclear grooves
activation of tyrosine kinase receptor

121
Q

Thyroid cancer associated w/ activation of tyrosine kinase receptor(2)

A

Papillary carcinoma

Medullary thyroid carcinoma

122
Q

Risk of papillary thyroid carcinoma increases w/ (2)

A

smoking

childhood radiation Rx

123
Q

Gene mutation in Ret oncogene in which thyroid carcinoma?

Also associated? (2)

A

Papillary thyroid carcinoma

NTRK1 mutation
BRAF gene

124
Q

Most common mutation in the BRAF gene for thyroid carcinoma (serene/threonine kinase)

125
Q

commonly associated thyroid cancer w/ either RAS or PAX8-PPAR mutation

A

follicular carcinoma

126
Q

cancer arising from the parafollicular C cells

secretes?

A

Medullary thyroid cancer

Calcitonin

127
Q

Follicular carcinoma vs adenoma

A

whether or not the fibrous capsule has been pierced or not

spreads hematogenousle

128
Q

Medullary carcinoma is located where?

Associated w?(2)

A

parafollicular C cells
-secretes calcitonin

Associated w MEN2A and MEN 2B

129
Q

Have a hard single fibrous nodule in an older patient be concern w?

A

undifferentiated/anaplastic carcinoma vs reidels in a younger patient

130
Q

Sheets of cells in an amyloid stroma

A

medullary thyroid carcinoma

131
Q

2 thyroid tumors associated w/ RET mutation

A

medullary carcinoma
papillary carcinoma

both tyrosine kinase activators as well

132
Q

Thyroid tumor complications (2)

A

hypocalcemia due to parathyroid removal

hoarseness w/ damage of the recurrent laryngeal nerve

133
Q

parafolliciluar cells secrete?

located?

A

calcitonin

located the medullary of the thyroid

Associated w/ medullary thyroid carcinoma

134
Q

Endocrine pancreas cell types and products (3)

A

Glucagon from the alpha cell
insulin from the beta cell
Somatostatin from the delta cell

135
Q

Glut 2 transporter found where(4) and responsible for

A

pancreatic beta cells
small intestine
liver
renal

responsible for glucose sensitivity,
insulin independent
bidirectional

136
Q

Glut 4 transporter found where(2) and responsible for

A

Adipose
skeletal

Responsible for insulin sensitive take-up of glucose

137
Q

GLUT 1 transporter found where? (2) responsible for

A

RBCs and the brain

responsible for insulin independent take of glucose

138
Q

Insulin receptor is what what type

A

tyrosine kinase leading to increase of GLUT 4 taken in

139
Q

How is insulin released from the beta pancreatic cell (6 steps)

A

increase in glucose -> Glut 2

  • > aerobic glycolysis -> increase of ATP/ADP ratio
  • > closing of ATP sensitive K cells
  • > depolarization of cell membrane
  • > opening of Voltage gated Ca channels and influx
  • > vesicles containing insulin fusing and leaving
140
Q

Results anabolic effects of insulin (4)

A

increase of glucose transport in skeletal muscle
increase in glycogen synthesis
increase in triglyceride synthesis
increase in protein synthesis

141
Q

Results of glucagon catabolism(4)

A

glycogenolysis
gluconeogenesis
lipolysis
-> ketone body production

mobilize stored energy and eventually increases insulin secretion

142
Q

Presentation of DM (5)

A

polydipsia
polyuria
polyphagia w/ weight loss (unable to get sugar in)
hyperglycemia

143
Q

2 main pathologies of Diabetes

A

Nonenzymatic glycosylation

  • small vessel disease: retinopathy and nephropathy
  • large vessel disease: atherosclerosis, gangrene

Osmotic Damage

  • neuropathy
  • cataracts
144
Q

Protective drug w/ nephropathy

A

ACE inhibitors

145
Q

Nonenzymatice glycosylation in DM leads to (3)

A

Small vessel disease
retinopathy
- hemmorage, exudates, microneurysms(flame)

nephropathy
-nodular sclerosis (kimmerstiel wilson nodules)

Large vessel disease

  • gangrene
  • Atherosclerosis
  • cerebrovacular disease
146
Q

Osmotic damage in DM is due to presence of what enzyme and lack of another in what organs (4)

A

have in aldose reductase, glucose -> sorbitol
Deficient in sorbitol dehydrogenase

Not in Retina, lens, schwann cells, kidney

147
Q

HLA DR3 -DQ2 and HLA DR4 DQ 8 are associated w/

148
Q

Which DM has a strong hereditary predisposition?

A

DM type II

149
Q

DKA is associated w/ what DM?

150
Q

Hyperosmolar hyperglycemic state is associated w/ what DM?

151
Q

Auto antibodies against GAD?

152
Q

What are some common causes of DKA?(7)

A 
Infection- pneumonia, gastroenteritis, UTI
diabetic med reduction/omission
severe medical illness  - MIC/CVA/truma
Undiagnosed DM
Dehydration
Alcohol/drug use
Corticosteriods

all mobilize stressors -> excess glucagon, catecholamine, cortiosteriods

153
Q

Pathogenesis of DKA?

A

increased insulin requirements due to tstressors. body goes to plan B (gluconeogen/lipolysis etc) to get sugar into cells despite plenty of sugar around in the serum

-excess fat breakdown
-beta oxidation overwhelms w/ acetyl coA
-ketogenesis
> beta hydroxybutyrate than acetoacetate

154
Q

Symptoms of DKA (6)

A 
kussmaul breathing
N/V
Abdominal pain
psychosis
dehydration
fruity odor
155
Q

Labs in DKA

H?
K?
sugars

A

hyperglycemia >300 mg/dL

metabolic acidosis w/ anion gap- give insulin till corrected
hyperkalemia (cells attempt to correct acidosis), polyuria -> net loss of K

156
Q

Insulin is needed in DKA for 2 things

A

Lower glucose sugars

correct the metabolic acidosis prevent further ketone formation

157
Q

Complications of DKA

A

murcomycosis - life threatening fungal infection
cerebral edema
cardiac arrythmia (w/ low K)-> V tach and torsades (low Mg)

158
Q

initial treatment of DKA (3)

A

IV fluids
IV insulin
IV K (repleat stores)

159
Q

why is DKA less common in Type II DM

A

because a little bit of insulin is available to prevent lipolysis and associated ketone generation

160
Q

Labs in hyperosmolar hyperglycemia state?

A

hyperglycemia (>800)
hyperosmolar >340

in type II DM

161
Q

mental confustion, delerium severe dehydration, N/V, ab pain, high sugars but no fruity breath

A

hyperosmolar hyperglycemic state

162
Q

Why are some type II DM capable of having ketosis

A

hereditary predisposition to toxic production that shuts down pancreatic secretion

163
Q

Lactic acidosis is a rare but worrisome side effect w/ this DM drug

164
Q

DMII Drug contraindicated w/ creatine >1.5

165
Q

Most common SFx of DMII drug is hypoglycemia

A

sulfonylureas

166
Q

DMII drug that is not safe in settings of hepatic dysfunction or CHF

A

Glitazones/thiazolinediones

pieoglitazone
rosiglitazone

167
Q

DMII Drugs that should not be used in patients w/ cirrhosis or inflammatory bowel disease

A

alpha glucosidase

Acarose
miglitol

168
Q

DMII drugs not associated w/ weight gain (3)

A

metformin

GLP1 Inhibitors

DPP4 inhibitors

169
Q

DMII drugs metabolized by the liver; excellent for patients w/ kidney disease

A

Thiazolidineodiones

170
Q

DMII drugs good for weight loss

A

GLP 1 analogs

171
Q

DMII medication that lowers LDL and triglercides as a bonus

172
Q

GLP 1 analogs (2)

A

exenatide

liraglutide

173
Q

sulfonureas (3)

A

glyburide
glimepride
glipizide

174
Q

DPP4 inhibitors (3)

A

linagliptan
saxagliptan
sitagliptan

175
Q

Metabolic syndrome 5 categories

A

Abdominal obesity - waist > 40 in males; >35 females
BP > 130/85
HDL < 40mg/dL male- 150 mg/dL
Fasting glucose >100

176
Q

Meds linked to increase hunger (4)

A 
Atypical antipsychotis
miratzapine
Several DM drugs
- insulin/TZD/ sulfonuresas
Progestins
177
Q

Common causes of nonalcoholic steatohepatitis(4)

pathogenesis

A

obesity, Type II DM, hyperlipidemia, insulin resisitance

the resistance -> lipid accumulation in the liver -> inflammation and PMN infiltration

progression fatty liver disease -> steatohepatitis -> cirrosis

178
Q

Diagnose fatty liver disease (2)

A

Imaging

  • US
  • CT
  • MRI
  • Magnetic resonance spectoscopy

Liver biopsy-> only those at risk for progression

179
Q

Rx for fatty liver disease (5)

A 
avoid alcohol
weight loss
control DM
TZDs -pioglitazone, improves LFTs and possibly histology
Metformin shows improvement
180
Q

BMI formula

A

Weight in kg / (height in meters)^2

181
Q

Hormone released by adipocytes regulating hunger

Acts where (2)

A

Leptin

in the hypothalamus

  • inhibits Lateral nucleus
  • stimulates VMN
182
Q

5 hypothalamus nuclei imlplicated in hunger

A

paraventricular nuclei
arcuate nuclei
Dorsal medial nucleus -stimulates GI

Lateral area (hunger, leptin inhibits)
ventromedial area (satiety, leptin stimulates)
183
Q

Lipodystrophy is what and could be due to ?

A

aplasia and distortion of the architecture of adipocytes
- ex: buffalo hump

Can be due to

  • HIV medications (protease inhibitors)
  • leptin deficiency
184
Q

Causes of hypercalcemia (7)

A

Primary hyperparathyroidism(90%)

  • solitary parathyroid adenoma (MEN1?)
  • parathyroid hyperplasia (MED2a?)

Maligancy

  • PTHrP (squamous cell, renal cell, breast METs to bone)
  • multiple myeloma
Excess Vitamon D ingestion
milk alkali syndrome - antacid ingestion
granulomatous disease (sarcoid/TB- macrophage Vit D)
Increased bone turn over
Thiazides
185
Q

Sympathetic cervical ganglia controls the parathyroids how?

A

controlling the bloodflow to the region

186
Q

what cell secretes Calcitonin?

PTH?

A

calcitonin - c cells/parafollicular in the thyroid

PTH - chief cells in the parathyroid

187
Q

3 ways PTH raises Ca

A

increases reabsorption in the bone (w/phosphate)
increases reabsorption in the kidney (distal convoluted tubule)
increase 1 alpha hydroxylase activity -> Vit D3 (calcitriol)

188
Q

Regulation of PTH
Ca?

Mg?

A

Ca sensors on chief cells respond to low serum levels

low Mg levels also stimulate PTH release but prolonged low Mg leads to less PTH

189
Q

Low Mg can affect what hormone?

Causes

A

PTH

diarrhea, aminoglycoside, diuretics, alcohol abuse

190
Q

How does PTH increase Ca reabsorption from the bone

A

binds to osteoblasts which up regulate RANK L which then binds to osteoclasts stimulating Ca release

191
Q

PTH role on phosphate?

A

Phosphate trashing hormone

192
Q

Vitamin D’s roll on Ca and phosphate (3)

A

Vitamin D increases Ca and Phosphate reabsorption from the gut

Vitamin D increases bone reabsorption of Ca and Phosphate

low Ca and Phosphate stimulate active Vit D

193
Q

Ca and Phosphate differences w/ Vit D and PTH

A

Vit D
-increases Ca and phosphate reabsorption in the gut

PTH increases only Ca reabsorption in the gut

194
Q

Most common cause of hypercalcemia ?

Consequences(4)

A

Stones
-renal stones/nephrocalcinosis/polyuria/uremia

Bones
-osteitis fribrosa cystica/osteoperosis/osteomalacia/osteoarthritis

Groans
-ab pain/constipation/peptic ulcers/pancreatitis

Psychiatric overtones
-lethargy/fatigue/depression/psychosis/ confusion

195
Q

Malignancies associated w/ PTHrP

A

Squamous cell - lung
renal cell carcinoma
Breast cancer to METs

196
Q

Why do you get peptic ulcers w/ hypercalcemia

A

stimulates gastrin production

197
Q

four conditions associated w/ hypercalcemia

A

Stones
-renal stones/nephrocalcinosis/polyuria/uremia

Bones
-osteitis fribrosa cystica/osteoperosis/osteomalacia/osteoarthritis

Groans
-ab pain/constipation/peptic ulcers/pancreatitis

Psychiatric overtones
-lethargy/fatigue/depression/psychosis/ confusion

198
Q

primary hyperparathyroidsm and secondary hyperparathyroidism have an increased lab value

199
Q

primary hyperparathyroidism lab value

Ca
alk phos
PTH
phosphate

A

High Ca
High Alk phos
High PTH
Low phosphate

200
Q

secondary hyperparathyroidism lab value

Ca
alk phos
PTH
phosphate

A

Low Ca (drives PTH release)
alk phos is high
PTH is high
Phos is high (due to inability to excrete despite high PTH)

common cause is chronic renal failure, due to decrease gut Ca reabsorption and increased phosphate

201
Q

most common cause of secondary hyperparathyroidism

A

chronic renal failure

202
Q

refractory hyperparathyroidism is due to

lab values of Ca?

A

due to chronic renal failure, very high PTH despite having high Ca

203
Q

Hypocalcemia is due to (4)

A

hypoparathyroidism

  • accidental removal of parathyroids
  • autoimmune destruction
  • Degeorge
  • Pseudohypoparathyroidism - kidneys unresponsive to PTH

Poor Ca intake

Vit D deficiency

Acute pancreatitis (Ca precipitates out FA -> soaps and excreted)

204
Q

Causes of hypo parathyroidism -> hypocacemia

A

Accidental removal
autoimmune destruction
pseudohypoparathyroidism
DeGeorge syndrome

205
Q

Pseudohypoparathyroidism due to?

See presentation?

Lab values of Ca and PTH

A

Albrights hereditary ostreodystophy

AD kidney unresponsive to PTH

  • > High PTH
  • > Low Ca due to loss in the kidney

shortened 4th and 5th digits
short stature
osteritis fibrosis cystica

206
Q

what starts the intrinsic pathway?

A

release of tissue factor from a cell binding to factor VII

207
Q

Thrombin does what in the coag pathway

what creates it?

A

prothrombin(factor II) -> thrombin via Xa
- Factor V serves as an excellent

thrombin converts fibrinogen to fibrin to create a mesh and stabilize clots

208
Q

what blocks Thrombin?

Which drug stimulates this effect?

A

Antithrombin (antithrombin III)

heparin induces

209
Q

Factor 12 encourages what 2 paths

A
  1. starts the intrinsic pathway and begins its shut down
  2. encourages conversion of prekallikrien -> kallikrein

kallikrein then
1. converts plasminogen -Plasmin
2.converts HMWK -> bradykinin
(vasodialation, permeability, pain)

210
Q

where does bradykinin come from and what are its effects(3)?

Breakdown due to?

A

Kallikrien encourages conversion of HWMK -> bradykinin

  • Vasodialation
  • Permeability
  • pain

Broken down by ACE enzyme

211
Q

Hemophilia A is deficient in ?

Hemophilia B is deficient in ?

Alters PTT and PT how

A

A - 8
B - 9

longer PTT time w/ intrinsic factor modulation
no change in PT

212
Q

Coagulation factors that serve as accelerants?

Modulator coag?

A

Factor 8a helps factor 9a activate factor 10 in the intrinsic pathway

Factor Va helps convert X -> Xa

Protein C and S deactivate the accelerants

213
Q

Kallikrien’s 2 functions

A
  1. increases conversion of HMWK -> bradykinin

2. increases conversion of plasminogen ->plasmin

214
Q

What additional components are needed in the coagulation cascade to assist (2)

A

Ca

phospholipids

215
Q

PT measures what?

What is normal

A

measures the amount of time to clot after addition of tissue factor ( the extrinsic pathway -> uniquely VII) in addition to common path

1 is a normal INR

216
Q

PTT measures what?

What is normal

A

PTT measures the amount of time to clot after adding something like silica, measures the intrinsic pathway (uniquely 12, 11, 9, 8) in addition to common path

normal is 35-40 seconds

217
Q

Vitamin K deficiency has an effect on what coag factors?

What happens to PTT and PT?

A

Factors C, S
10, 9, 7, 2 are deficient

BOTH PTT and PT are elevated

218
Q

macrohemmorrage such as hemarthrosis and easy bruising are due to defects in what?

A

coagulation cascade like hemophilia A or B

219
Q

Factor V leiden deficency presents as?

Due to

A

most common form of hypercoagability

Factor 5 is mutated so protein C cannot shut down the cascade-> hypercoagable

220
Q

Prothrombin G20210A is

A

G20210A

mutation in the 3’ untranslated region of adenosine to guanine in prothrombin gene leading to increase production of prothrombin and hypercoagability

221
Q

2 less common states of hypercoagability after factor V leiden and Prothrombin mutation?

A

Protein C/S deficiency -> less to inactivate factor V

Antithrombin deficiency -> less to inactivate Thrombin

222
Q

What hypercoagable state may not be helped w/ thrombin?

A

antithrombin deficiency

223
Q

Preferred anticoagulant during pregnancy?

A

Heparin or LMWH

224
Q

Use of Heparin?

A

Immediate anticoag desired

  • PE
  • Acute coronary
  • MI
  • DV

Pregnancy

225
Q

Platelets are decreasing after a new medication post an MI what is the drug?

MOA of toxicity

A

Heparin

Heparin induced thrombocytopenia, -> IgG antobodies bind to Heparin bound to Platelet factor 4

  • > activation and clumping (hypercoagable)
  • > eventual removal -> thrombocytopenia
226
Q

Low molecular weight heparins (2)

A

enoxaparin
dalteparin

act more on factor Xa than antithrombin inducing

have better bioavailability

227
Q

Toxicity w heparin (3)

Rx?

A

Bleeding
thrombocytopenia (Heparin induced thrombocytopenia)
osteoperosis

protamine sulfate

228
Q

direct Xa blockers (2)

A

Argatroban

dabigatron

229
Q

hirudin derived anticoags (3)

A

pepirudin
bivalirudin
desirudin

works by inhibiting thrombin ~ to natural antithrombin but dif MOA

230
Q

skin tissue necrosis after a DVT be suspicious of what recently added drug?

Rx?

A

Warfarin

Give K either oral/IV

Fresh frozen plasma for immediate help

231
Q

Follow what labs w/ warfarin?

w/ Heparin

A

follow INR/PT w/ warfarin

follow PTT w/ Heparin

232
Q

Thrombolytics (4)

A

alteplase (tPA)
reteplase
tenecteplase
streptokinase

233
Q

Clinical use of thrombolytic

see what lab values w/ PTT and PT?

A

converts plasminogen -> plasmin
-> increase PTT and PT

used in early MI (if no cath lab), early stroke, thrmbolysis of PE

234
Q

Toxicity of thrombolytic

Rx

A

bleeding - do not use w/ a history of:

  • recent surgery
  • known bleeding dysarthria,
  • HTN
  • intracranial bleeding

Aminocapronic acid

USLME Kiss my ass and pray (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions