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USMLE STEP 1 > Endo > Flashcards

Endo Flashcards

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1
Q

Thyroid development
Where does it arise from?
Where does it descend to?
Connected to what by what?

A

Thyroid diverticulum arises from floor of primitive pharynx. Descends into neck. Connected to tongue by thyroglossal duct, which normally disappears but may persist as pyramidal lobe of thyroid

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2
Q

Foramen Cecum

A

Normal remnant of thyroglossal duct in tongue

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3
Q

Most common ectopic thyroid tissue site

A

Tongue

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4
Q

Presentation of thyroglossal duct cyst

A

Anterior midline neck mass that moves with swallowing

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5
Q

Presentation of persistent cervical sinus leading to branchial cleft cyst in lateral neck

A

Small mobile mass on side of neck that does not move with swallowing

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6
Q

What does the Fetal Adrenal Gland consist of?

A

Outer adult zone and inner active fetal zone

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7
Q

Adult zone of fetal adrenal gland
Activity?
Control of activity?

A

Dormant during early fetal life but begins to secrete cortisol late in gestation
Fetal pituitary and placenta make ACTH and CRH

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8
Q

What is fetal cortisol responsible for?

A

Fetal lung maturation and surfactant production

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9
Q

Embryological origin of adrenal cortex?

A

Mesoderm

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10
Q

Embryological origin of adrenal medulla?

A

Neural Crest Cells

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11
Q

Layers of Adrenal Gland w/ Secretory Products

A

“GFR –> Salt, Sugar, Sex
Deeper you go, the sweeter it gets”
Capsule
Zona Glomerulosa –> Aldosterone
Zona Fasciculata –> Cortisol, Sex Hormones
Zona Reticularis –> Sex Hormones (androgens)
Medulla –> Catecholamines (NE, Epi)

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12
Q

Zona Glomerulosa
Responsive to
Secretory Product

A

Renin-Angiotensin –> Aldosterone

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13
Q

Zona Fasciculata
Responsive to
Secretory Product

A

ACTH, Hypothalamic CRH –> Cortisol, Sex Hormones

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14
Q

Zona Reticularis
Responsive to
Secretory Product

A

ACTH, Hypothalamic CRH –> Sex Hormones (androgens)

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15
Q

Adrenal Medulla
Responsive to
Secretory Product

A

Preganglionic sympathetic fibers –> ACh –> Catecholamines (NE, Epi)

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16
Q

Most common tumor of adrenal medulla in adults?

A

Pheochromocytoma

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17
Q

Most common tumor of adrenal medulla in children?

A

Neuroblastoma

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18
Q

Pheochromocytoma vs Neuroblastoma in terms of clinical presentation

A

P –> episodic HTN

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19
Q

Adrenal gland venous drainage

A

L Adrenal –> L Adrenal Vein –> L Renal Vein –> IVC

R Adrenal –> R Adrenal Vein –> IVC

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20
Q 
Posterior Pituitary Gland
AKA
Products 
Source of products?
How are they transported?
Embryological origin
A

Neurohypophysis
Secretes ADH and Oxytocin made in hypothalamus and shipped to PP via neurophysins (carrier proteins)
Derived from neuroectoderm

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21
Q

Anterior Pituitary Gland
AKA
Secretory Products
Embryological origin

A

Adenohypophysis
“My FLAT PiG”
Melanotropin (MSH), FSH, LH, ACTH, TSH, Prolactin, GH
Derived from oral ectoderm (Rathke’s Pouch)

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22
Q

Acidophils in the Anterior Pituitary gland secrete

A

GH and Prolactin

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23
Q

Basophils in the Anterior Pituitary gland secrete

A

“B FLAT”

Basophils –> FSH, LH, ACTH, TSH

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24
Q

Which hormones share the same α subunit?

A

FSH, LH, TSH, and hCG

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25
Q

Endocrine Pancreas
Name
Cell types: Products and Location
Embryological origin?

A 
Islets of Langerhans 
"INsulin is on the INside" 
α: Glucagon, Peripheral  
β: Insulin, Central
δ: Somatostatin, Interspersed 
Pancreatic Buds
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26
Q

Mechanism of Insulin Release

A

↑ Glucose metabolism –> ↑ ATP –> closing of K channels –> depolarization –> V gated Ca channels open –> insulin secretion

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27
Q

Does insulin cross the placenta?

A

No

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28
Q

What organs take up glucose independently of insulin?

A

“BRICK L”

Brain, RBCs, Intestines, Cornea, Kidney, Liver

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29
Q

GLUT1

A

Insulin independent in Brain and RBCs

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30
Q

GLUT2

A

Bidirectional in β cells, liver, kidney, and small intestine

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31
Q

GLUT4

A

Insulin dependent in adipose tissue and skeletal muscle

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32
Q

Effects of Insulin

A 
Anabolic 
↑ G transport into skeletal muscles and adipose tissue 
↑ Glycogen synthesis and storage
↑ Triglyceride synthesis and storage 
↑ Na retention by kidneys
↑ Protein synthesis in muscles 
↑ K uptake by cells
↑ AA uptake by cells
↓ Glucagon release
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33
Q

What triggers an ↑ in insulin release

A

Hyperglycemia
GH (via insulin resistance)
β2 agonists

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34
Q

What triggers a ↓ in insulin release

A

Hypoglycemia, Somatostatin, α2 agonists

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35
Q

Insulin Receptor Cellular Pathway

A

Insulin –> Tyrosine Phosphorylation –> IP3 and RAS/MAP
IP3 –> Glycogen, Lipid, + Protein synthesis and GLUT4 vesicle mobilization
MAP/RAS –> Cell Growth and DNA synthesis

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36
Q

What does the brain use for energy during starvation?

A

Ketone bodies

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37
Q

What do RBCs use for energy during starvation

A

RBCs can only use glucose b/c they cannot preform aerobic respiration

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38
Q

Functions of Glucagon

A

Catabolic

↑ Gluconeogenesis, Glycogenolysis, Lipolysis, Ketone production

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39
Q

What is glucagon secreted in response to?

A

Hypoglycemia

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40
Q

What inhibits glucagon production?

A

Insulin, Hyperglycemia, Somatostatin

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41
Q

What does TRH do?

A

TRH –> TSH and Prolactin

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42
Q

What does DA do in the Pituitary gland?

A

DA –/ prolactin

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43
Q

What does CRH do?

A

CRH –> ACTH, Melanocyte Stimulating Hormone (MSH), β-endorphin

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44
Q

What does GHRH do?

A

GHRH –> GH

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45
Q

What does somatostatin do in the Pituitary?

A

Somatostatin –/ GH and TSH

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46
Q

What does GnRH do?

A

GnRH –> FSH and LH

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47
Q

What does Prolactin do in the pituitary?

A

Prolactin –/ GnRH

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48
Q

Prolactin
Source
Function in Breast
Function in Pituitary

A

Anterior Pituitary Gland
Stimulates milk production in breasts
Prolactin –/ GnRH synthesis and release which leads to an inhibition of ovulation and spermatogenesis

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49
Q

Regulation of Prolactin Secretion

A

DA from Hypothalamus –/ Prolactin secretion from Anterior Pituitary
Prolactin in turn increases DA synthesis and secretion in the Hypothalamus thereby inhibiting its own secretion
TRH –> Prolactin secretion

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50
Q

Affects of DA agonists on prolactin?

A

DA agonists (bromocriptine) inhibit prolactin and can be used to treat prolactinoma

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51
Q

What stimulates prolactin secretion?

A

TRH, DA antagonists (antipsychotics) and Estrogens (OCP, pregnancy)

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52
Q 
Growth Hormone
Name
Source
Function and MoA
Pattern of release
Regulation
A

Somatotropin
Anterior Pituitary Gland
Stimulates linear growth and muscle mass through IGF1/somatomedin secretion
↑ Insulin Resistance (Diabetogenic)
Pulsatile release in response to GHRH
Secretion ↑ during exercise and sleep
Secretion inhibited by glucose and somatostatin

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53
Q

Excess GH in adults vs children

A

Acromegaly in adults

Gigantism in children

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54
Q

Desmolase
Regulation
Action

A

ACTH –> Desmolase
Ketoconazole –/ Desmolase
D turns Cholesterol into Pregnenolone

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55
Q

Path of Aldosterone Synthesis

A

Pregnenolone –> [3β Hydroxysteroid dehydrogenase] –> Progesterone –> [21 hydroxylase] –> 11 deoxycorticosterone –> [11β hydroxylase] –> corticosterone –> [aldosterone synthase] –> Aldosterone

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56
Q

Path of Cortisol Synthesis

A

Pregnenolone –> [17α hydroxylase] –> 17 hydroxypregnenolone –> [3β Hydroxysteroid dehydrogenase] –> 17 hydroxyprogesterone –> [21 hydroxylase] –> 11 deoxycortisol –> [11β hydroxylase] –> Cortisol
or…
Pregnenolone –> [3β Hydroxysteroid dehydrogenase] –> Progesterone –> [17α hydroxylase] –> 17 hydroxyprogesterone –>

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57
Q

Path of Testosterone and DHT production

A

Pregnenolone –> [17α hydroxylase] –> 17 hydroxypregnenolone –> Dehydroepiandrosterone (DHEA) –> [3β Hydroxysteroid dehydrogenase] –> Androstenedione –> Testosterone –> [5α reductase] –> DHT
or…
17 hydroxyprogesterone –> Androstenedione

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58
Q

Synthesis of Peripheral Estrogens

A

Aromatase turns Androstenedione into Estrone
Aromatase turns Testosterone into Estradiol
Estrone can convert to Estradiol

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59
Q

Deficiencies in Bilateral Adrenal Hyperplasias

A

17α hydroxylase, 21 hydroxylase, 11β hydroxylase

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60
Q

Why do adrenal enzyme deficiencies lead to hyperplasia

A

↑ ACTH stimulation because of ↓ cortisol

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61
Q 
17α hydroxylase deficiency 
Mineralcorticoids
Cortisol
Sex Hormones
Presentation
Male vs Female
A

Mineralcorticoids ↑
Cortisol ↓
Sex Hormones ↓
HTN, HypoK
Male: ↓ DHT –> pseudohermaphroditism (variable, ambiguous genitalia with undescended testes)
Female: Externally phenotypic female with normal internal sex organs but lack secondary sex characteristics

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62
Q 
21 hydroxylase deficiency 
Mineralcorticoids
Cortisol
Sex Hormones
Presentation
A

Mineralcorticoids ↓
Cortisol ↓
Sex Hormones ↑
Hypotension, HyperK, ↑ Renin activity, Volume depletion
Masculinization leading to pseudohermaphroditism in females

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63
Q 
11β hydroxylase deficiency 
Mineralcorticoids
Cortisol
Sex Hormones
Presentation
A 
Mineralcorticoids:
↓ Aldosterone, ↑ 11-deoxycorticosterone 
Cortisol ↓ 
Sex Hormones ↑
HTN, Masculinization
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64
Q

Cortisol
Source
Function
Regulation

A 
Adrenal Zona Fasciculata 
"BBIIG"
Maintains BP
↓ Bone formation
↑ Insulin Resistance 
AntiInflammatory/Immunosuppressive 
↑ Gluconeogenesis, lipolysis, proteolysis 
Inhibits Fibroblasts --> striae 
CRH (hypothalamus) --> Anterior Pituitary --> ACTH --> Cortisol production in Zona Fasciculata
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65
Q

How is cortisol transported in the blood?

A

Corticosteroid binding globulin (CBG)

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66
Q

How does cortisol maintain BP?

A

Upregulates α1 receptors on arterioles –> ↑ sensitivity to NE and Epi

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67
Q

How is cortisol an anti-inflammatory/immunosuppressive?

A

–/ production of leukotrienes and prostaglandins
–/ leukocyte adhesion
–/ histamine release
Reduces eosinophils
–/ IL2 production

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68
Q

How does excess cortisol alter CRH, ACTH and Cortisol secretion

A

Decreases all of them

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69
Q

How does chronic stress affect cortisol secretion?

A

Stress induces prolonged secretion

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70
Q

PTH
Source
Function

A 
Chief Cells of Parathyroid 
↑ Bone resorption of Ca and PO4
↑ Kidney reabsorption of Ca in DCT
↑ Calcitriol production by stimulating kidney 1α Hydroxylase  
↓ Reabsorption of PO4 in PCT
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71
Q

Regulation of PTH

A

↓ Serum Ca –> ↑ PTH
↓ Serum Mg –> ↑ PTH
↓↓ Serum Mg –> ↓ PTH
↑ Vit D –> ↓ PTH

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72
Q

Common causes of ↓ Mg

A

Diarrhea, Aminoglycosides, Diuretics, EtOH abuse

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73
Q

Number of Parathyroid glands

A

4 glands

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74
Q

How does PTH affect bone

A

Stimulate Ca release from bone mineral compartment
Stimulates osteoblastic cells
Stimulates bone resorption via indirect effect of osteoclasts
Enhances bone matrix degradation

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75
Q

Actions of Vit D

A

↑ Intestinal absorption of Ca and PO4
↑ Release of PO4 from bone matrix
↑ Bone resorption of Ca and PO4

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76
Q

Clinical manifestation of high PTH

A

↑ serum Ca, ↓ serum PO4, ↑ urine PO4

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77
Q

How does PTH affect osteoblasts and osteoclasts

A

PTH –> ↑ production of M-CSF and RANK-L in osteoblasts which stimulates osteoclasts

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78
Q

Source of Vit D

A

D3 from sun exposure in skin
D2 ingested from plants
Both converted to 25-OH in liver and 1,25-(OH)2 in the kidney

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79
Q

Regulation of Vit D

A

↑ PTH, ↓ [Ca], ↓ PO4 –> ↑ VitD

↑ Vit D inhibits its own production

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80
Q

24,25-(OH)2 D3

A

Inactive form of VitD

81
Q

VitD deficiency in adults vs children

A

Children –> rickets

Adults –> osteomalacia

82
Q

Calcitonin
Source
Function
Regulation

A

Parafollicular cells (C cells) of thyroid
↓ bone resorption of Ca
↑ serum Ca –> calcitonin secretion

83
Q

Normal role of Calcitonin

A

“CalciTONin TONes down Ca levels”

Not important in normal Ca homeostasis but when active, opposes PTH

84
Q

Which hormones use cAMP

A

“Go Go FLAT ChAMP”

GHRH, Glucagon, FSH, LH, ACTH, TSH, CRH, Calcitonin, ADH (V2 receptor), MSH, PTH

85
Q

Which hormones use cGMP

A

“Vasodilators”

ANP, NO, EDRF (Endothelial Derived Relaxing Factor)

86
Q

Which hormones use IP3

A

“HAG GGOAT”

Histamine (H1), Angiotensin II, Gastrin, GnRH, Oxytocin, ADH (V1 receptor), TRH

87
Q

Hormones that use steroid receptors

A

“VETTT CAP”

VitD, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone

88
Q

Hormones that use Intrinsic Tyrosine Kinases

A

“MAP kinase pathway - Think growth factors”

Insulin, IGF1, FGF, PDGF, EGF

89
Q

Hormones that use Receptor-Associated (Non-Receptor) Tyrosine Kinase

A

JAK/STAT pathway
Think Acidophiles and cytokines - “PIG”
Prolactin, Immunomodulators (cytokines IL2, IL6, IL8, IFN), GH

90
Q

In men, what are the effects of ↑ sex hormone binding globulin

A

Lowers free testosterone –> gynecomastia

91
Q

In women, what are the effects of ↓ sex hormone binding globulin

A

Raises free testosterone –> hirsutism

92
Q

In a women, what happens to SHBG during pregnancy?

A

↑ SHBG

93
Q

Thyroid Hormone
Formulations
Source

A

T3 and T4

Follicles of thyroid. Most T3 is formed in target tissues

94
Q

Function of Thyroid Hormone

A

T3 –> 4 Bs
Brain maturation
Bone Growth (synergism with GH)
β adrenergic effects: ↑ β1 receptors in heart –> ↑ CO, HR, SV, and contractility
↑ Basal metabolic rate: ↑ Na/K ATPase activity –> ↑ O2 consumption, RR, body Temp
↑ glycogenolysis, gluconeogenesis, lipolysis

95
Q

How is TH transported in the blood

When is it active?

A

Thyroxine binding globulin binds most T3/T4 in blood

Only free hormone is active

96
Q

When does TBG levels change?

A

↓ TBG in hepatic failure

↑ TBG in pregnancy or OCP (estrogen ↑ TBG)

97
Q

What is the major thyroid product?
What is it converted into?
Where is it converted?
What converts it?

A

T4

Converted to T3 in peripheral tissues by 5’-deiodinase

98
Q

Which thyroid product binds with greater affinity?

A

T3

99
Q

Peroxidase in Thyroid

A

Oxidation and organification of Iodide as well as coupling of MIT and DIT

100
Q

Propylthiourcil
MoA
Use
Tox

A

Inhibits Peroxidase and 5’-deiodinase
Hyperthyroidism
Tox: skin rash, agranulocytosis, aplastic anemia, hepatotoxicity

101
Q

Methimazole
MoA
Use
Tox

A

Inhibits Peroxidase
Hyperthyroidism
Tox: skin rash, agranulocytosis, aplastic anemia, teratogen

102
Q

Thyroid Hormone Regulation

A

Hypothalamus –> TRH –> Pituitary –> TSH –> Follicular cells of thyroid gland –> TH
Negative feedback by T3 to anterior pituitary ↓ sensitivity to TRH

103
Q

Wolff-Chaikoff Effect

A

Excess I temporarily inhibits thyroid peroxidase –> ↓ iodine organification –> ↓ T3/T4 production

104
Q

Function of Follicular Cells in Thyroid Gland

A

Take up I- and oxidize it to I2 for excretion into lumen. In lumen TG and I2 form MIT and DIT.
Take up TG and proteolysis occurs to release T3/T4

105
Q

Cushing’s Syndrome
Primary Pathophysiology
Different kinds of causes

A

↑ cortisol

Exogenous vs Endogenous causes

106
Q

1 cause of Cushing’s syndrome?

A

Exogenous steroids –> ↓ ACTH

107
Q

Endogenous causes of Cushing’s Syndrome

A

Cushing’s Disease (70%): ACTH secretion from pituitary adenoma
Ectopic ACTH (15%): Non pituitary tissue makes ACTH (usually small cell lung cancer, bronchial carcinoids)
Adrenal (15%): adenoma, carcinoma, nodular adrenal hyperplasia. Low ACTH

108
Q

Presentation of Cushing’s Syndrome

A

HTN, Wt Gain, Moon facies, Truncal obesity, Buffalo hump, Hyperglycemia (insulin resistance), Skin changes (thinning, striae),peptic ulcers, osteoporosis, amenorrhea, immune suppression

109
Q 
Dexamethasone Suppression Test on Cortisol 
Normal
ACTH pituitary tumor
Ectopic ACTH producing tumor
Cortisol producing tumor
A 
Low dose                 High Dose
Suppressed              Suppressed
Remains ↑                Suppressed
Remains ↑                Remains ↑
Remains ↑                Remains ↑
110
Q 
Primary Hyperaldosteronism 
Causes
Presentation 
Distribution 
Treatment
A

Adrenal hyperplasia or aldosterone secreting adrenal adenoma (Conn’s Syndrome)
HTN, HypoK, Metabolic alkalosis, low Renin
Maybe bilateral or unilateral
Surgery to remove tumor and/or spironolactone

111
Q 
Secondary Hyperaldosteronism 
Pathophysiology
Underlying Causes
Associated with...
Treatment
A

Renal perception of low intravascular volume –> overactive Rennin-Angiotensin system
Due to Renal Artery Stenosis, Chronic Renal Failure, CHF, Cirrhosis, Nephrotic Syndrome
Associated with high Renin levels
Treat with Spironolactone

112
Q 
Addison's Disease
What is it?
Pathophysiology 
Presentation
Diseases that can lead to it
A

“Adrenal Atrophy and Absence of hormones from All 3 cortical layers”
Chronic primary adrenal insufficiency due to adrenal atrophy or destruction.
Deficiency in aldosterone and cortisol leads to hypotension (hyponatremic volume contraction), hyperK, acidosis, skin hyper-pigmentation
Autoimmune, TB, Metastatic Cancer

113
Q

Why is skin hyper-pigmented in Addison’s disease?

A

MSH, a byproduct of ACTH production from POMC, is elevated

114
Q

How is Primary adrenal insufficiency different from Secondary adrenal insufficiency

A

Secondary is from ↓ pituitary ACTH. No skin hyper-pigmentation and no hyperK

115
Q

Waterhouse-Friderichsen Syndrome
What is it?
What is it due to?
What conditions is it associated with?

A

Acute Primary adrenal insufficiency
Due to adrenal hemorrhage
Associated with Neisseria meningitidis septicemia, DIC, and endotoxic shock

116
Q 
Pheochromocytoma
Arise from
Most tumors secrete 
Findings 
Associated with what other diseases?
A

Arise from chromaffin cells (neural crest cells)
Most secrete Epi, NE, and DA
Episodic HTN, Urinary vanillyl mandelic acid (VMA), ↑ plasma catecholamines
Associated with neurofibromatosis type 1, MEN Type 2A and 2B

117
Q

Treatment of Pheochromocytoma

A

Tumor surgically removed only after effective α and β blockade is achieved
Irreversible α antagonists (phenoxybenzamine) must be given first to avoid hypertensive crisis. β blockers are then given to slow heart rate

118
Q

Symptoms of episodic HTN

A 
Pressure (elevated BP)
Pain (headache)
Perspiration
Palpitations (tachycardia)
Pallor
119
Q

Rule of 10 with Pheochromocytoma

A 
10% malignant 
10% bilateral
10% extra-adrenal 
10% calcify
10% kids
120
Q

Path of DA, NE and Epi synthesis

A

Phenylalanine –> Tyrosine –> L DOPA –> DA –> NE –> Epi

121
Q

Product of DA metabolism

A

HVA

122
Q

Product of NE and Epi metabolism

A

VMA

123
Q 
Neuroblastoma 
Frequency
Location
Findings 
Presentation 
Genetics
A

Most common tumor of adrenal medulla in children
Can occur anywhere along the sympathetic chain
HVA elevated in urine
HTN less likely to develop
Overexpression of N-myc oncogene associated with rapid tumor progression

124
Q 
Hypothyroidism 
Temp
Wt
Activity 
GI
Reflexes
Myxedema 
Skin
Hair
Heart
TSH
TH
A 
Cold intolerance
Wt Gain with ↓ appetite 
Hypoactivity, lethargy, fatigue, weakness
Constipation 
↓ reflexes 
facial/periorbital myxedema 
Dry cool skin
Coarse brittle hair
Bradycardia, SOBE
↑ TSH
↓ free T4
125
Q 
Hyperthyroidism 
Temp
Wt
Activity 
GI
Reflexes
Myxedema 
Skin
Hair
Heart
TSH
TH
A 
Heat intolerance 
Wt loss with ↑ appetite
Hyperactivity 
Diarrhea
↑ reflexes
Pretibial myxedema
Warm moist skin
Fine hair
Chest pain, palpitations, arrhythmias, ↑ β adrenergic receptors
↓ TSH (if primary)
↑ Free or total T3 and T4
126
Q 
Hashimoto's Thyroiditis 
Kind of thyroidism
Frequency 
Pathophysiology 
Genetics
Risk
Histology 
Physical exam
Course of disease
A

Hypothyroidism
Most common cause of hypothyroidism
Autoimmune disorder (thyroid peroxidase and anti thyroglobulin Abs)
Associated with HLA DR5
Increased risk of non-Hodgkin’s lymphomas
Hurthle cells, lymphocytic infiltrate with germinal centers
Moderately enlarged nontender thyroid
May be hyperthyroid early in course (thyrotoxicosis during follicular rupture)

127
Q

Cretinism
Kind of thyroidism
Pathophysiology with circumstances
Findings

A

Fetal Hypothyroidism
Endemic: Lack of dietary iodine
Sporadic: Defect in T4 formation or developmental failure in thyroid formation
Pot bellied, Pale, Puffy face, Protruding umbilicus and Protuberant tongue

128
Q 
Subacute Thyroiditis 
Name
Kind of thyroidism 
Description 
Usually follows
Histology 
Findings 
Course
A 
de Quervain's Hypothyroidism 
Self limited 
Often following flu like illness
Granulomatous inflammation
↑ ESR, Jaw pain, early inflammation, tender thyroid 
May be hyperthyroidism early in course
129
Q

Reidel’s Thyroiditis
Kind of thyroidism
Pathophysiology
Findings

A

Hypothyroidism
Thyroid replaced by fibrous tissue (considered a manifestation of IgG4 related systemic disease)
Fixed, hard, painless goiter

130
Q

Toxic multinodular goiter
Kind of thyroidism
PathoPhys
Malignant?

A

Hyperthyroidism
Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation of TSH receptor
Rarely malignant

131
Q

Jod-Basedow Phenomenon

A

Thyrotoxicosis if a pt with iodine deficiency goiter is made iodine replete

132
Q 
Graves' Disease
Kind of thyroidism
PathoPhys
Presentation 
Often presents during
A

Hyperthyroidism
Autimmune with thyroid stimulating immunoglobulins
Ophthalmopathy (proptosis, EOM swelling), pretibial myxedema, ↑ connective tissue deposition, diffuse goiter
Often presents during stress (childbirth)

133
Q 
Thyroid Storm
Kind of thyroidism
What is it?
What does it cause?
What causes it?
Findings
A

Hyperthyroidism
Stress-induced catecholamine surge leading to death by arrhythmia
Seen as a complication of Graves’ and other hyperthyroid disorders
↑ ALP due to increased bone turnover

134
Q 
Papillary Thyroid Carcinoma 
Frequency
Prognosis
Histology 
Predisposing factors
A

Most common thyroid cancer
Excellent prognosis
empty-appearing nuclei (Orphan Annie’s Eyes), Psammoma bodies, Nuclear grooves,
↑ risk with childhood radiation

135
Q

Follicular Thyroid Carcinoma
Prognosis
Histology

A

Good prognosis

Uniform follicles

136
Q 
Medullary Thyroid Carcinoma
Source 
What molecules does it produce?
Histology 
Associated with what other diseases
A

Parafollicular C cells
Produces calcitonin
Sheets of cells in amyloid stroma
Associated with MEN types 2A and 2B

137
Q

Undifferentiated/anaplastic thyroid cancer
Kind of pt?
Prognosis

A

Older pt with very poor prognosis

138
Q

What is thyroid lymphoma associated with?

A

Hashimoto’s Thyroiditis

139
Q

Primary Hyperparathyroidism
Usually caused by…
Findings
Symptoms

A

Usually an adenoma
HyperCa, Hypercalciuria (renal stones), ↑PTH, ↑ALP, ↑cAMP in urine
Often asymptomatic but can present with weakness and constipation

140
Q

Osteitis Fibrosa Cystica

A

↑ PTH –> Cystic bone spaces filled with brown fibrous tissue –> bone pain

141
Q

Secondary Hyperparathyroidism
What causes it?
Most often seen in what disease?
Findings

A

↓ Gut Ca absorption and ↑ Phosphate
Most often in chronic renal disease (low VitD)
HypoCa, HyperPO4 (in chronic renal disease), HypoPO4 (with other causes), ↑ALP, ↑PTH

142
Q

Renal Osteodystrophy

A

Bone lesion due to secondary or tertiary hyperparathyroidism due to renal disease

143
Q

Tertiary Hyperparathyroidism
What causes it?
Findings

A

Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease. ↑↑PTH and ↑ Ca

144
Q

Hypoparathyroidism
Causes
Findings

A

Surgical excision, autoimmune, DiGeorge Syndrome

HypoCa, Tetany, Chvostek’s Sign, Trousseau’s Sign.

145
Q

Chvostek’s Sign

A

Tapping of facial nerve –> contraction of facial muscles

146
Q

Trousseau’s Sign in Hypoparathyroidism

A

Occlusion of brachial artery w/ BP cuff –> carpal spasm

147
Q 
PseudoHypoparathyroidism
Name
Genetics
PathoPhys
Findings
A

Albright’s Hereditary Osteodystrophy
Autosomal dominant
Kidney unresponsive to PTH
HypoCa, Shortened 4th/5th digit, short stature

148
Q

Low Ca, High PTH

A

Secondary Hyperparathyroidism

149
Q

Low Ca, Low PTH

A

Hypoparathyroidism

150
Q

High Ca, High PTH

A

Primary Hyperparathyroidism

151
Q

High Ca, Low PTH

A

PTH independent HyperCalcemia

152
Q

Most common pituitary adenoma

A

Prolactinoma

153
Q

Prolactinoma
Findings
Treatment

A 
Amenorrhea, Galactorrhea, Low Libido, Infertility
DA agonist (bromocriptine or cabergoline)
154
Q

Common presentation of pituitary adenoma

A

Bitemporal hemianopia from impingement on optic chiasm

155
Q

Acromegaly
What is it?
What causes it?
Findings

A

Excess GH in adults
Typically caused by pituitary adenoma
Large tongue with deep furrows, Course facial hair, Insulin resistance

156
Q

Acromegaly
Diagnosis
Treatment

A

↑ serum IGF1; Failure to suppress serum GH following oral glucose tolerance test; Pituitary mass on MRI
Resection followed by somatostatin analog (Octreotide)

157
Q

Diabetes Insipidus
PathoPhys
Presentation

A

Central: Lack of ADH (pituitary tumor, trauma, surgery, histiocytosis x)
Nephrogenic: Lack of renal response to ADH (hereditary, hyperCa, Li, demeclocycline)
Thirst and Polyuria

158
Q

Diabetes Insipidus
Findings
Diagnosis
Treatment

A

Urine specific gravity < 1.006; Serum osmolality > 290
Water deprivation test (urine osmolality doesn’t ↑)
Response to desmopressin distinguishes central vs nephrogenic
Fluid intake. For central: intranasal desmopressin. For Nephrogenic: hydrochlorothiazide, indomethacin, or amiloride

159
Q 
SIADH
Characteristics 
Normal body response 
Dangerous complication 
Possible causes 
Treatment
A

Excess water retention, Low Na, Urine osmolarity > serum osmolarity
Body responds with ↓ aldosterone
Low Na can lead to seizures
Ectopic ADH (small cell lung cancer), CNS disorder, Head trauma, Pulmonary disease, Drugs (cyclophosphamide)
Fluid restriction, IV saline, Conivaptan, Tolvaptan, Demeclocycline

160
Q

Hypopituitarism
What causes it?
Treatment

A 
Nonsecreting pituitary adenoma, craniopharyngioma
Sheehan's Syndrome 
Empty Sella Syndrome 
Brain injury, hemorrhage
Radiation
Treat with substitution therapy
161
Q

Sheehan’s Syndrome

A

Postpartum ischemic infarct of pituitary. Usually presents with failure to lactate

162
Q

Empty Sella Syndrome

A

Atrophy or compression of the pituitary. Often idiopathic. Common in obese women

163
Q

Acute manifestations of Diabetes Mellitus

A

Polydipsia, Polyuria, Polyphagia, Wt loss, DKA (type1), HHS (type2), Unopposed secretion of GH and Epi (exacerbate hyperglycemia)

164
Q

Reason for coma and death in DM?

A

Dehydration and Acidosis

165
Q

Chronic manifestations of DM?

A

Nonenzymatic glycosylation and Osmotic damage

166
Q

Nonenzymatic Glycosylation in DM

A

Small Vessels: diffuse thickening of basement membrane –> retinopathy (hemorrhage, exudates, microaneurysm, vessel proliferation), glaucoma, nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to HTN, Kimmelstiel Wilson nodules)
Large Vessels: Atherosclerosis, CAD, Peripheral vascular occlusive disease, gangrene –> limb loss cerebrovascular disease

167
Q

Osmotic Damage in DM

A

Sorbitol accumulation in organs with aldose reductase
Neuropathy (motor, sensory, autonomic)
Cataracts

168
Q

Tests for DM

A

Fasting serum glucose
Oral GTT
HbA1C (3 months)

169
Q 
DM1
Defect
Insulin in treatment 
Age
Obesity
Genetics
HLA
Glucose intolerance 
Insulin sensitivity
Ketoacidosis 
β cell #
Serum insulin level
Classic symptoms 
Histology
A 
Autoimmune destruction of β cells
Insulin always used 
Pt <30
Not obese 
Weak genetic connection 
HLA DR3 and DR4
Severe glucose intolerance 
High insulin sensitivity 
Ketoacidosis common 
β cell # ↓
Serum insulin ↓
Classic symptoms common
Islet leukocytic infiltration
170
Q 
DM2
Defect
Insulin in treatment 
Age
Obesity
Genetics
HLA
Glucose intolerance 
Insulin sensitivity
Ketoacidosis 
β cell #
Serum insulin level
Classic symptoms 
Histology
A 
Insulin resistance with progressive β cell failure
Insulin sometimes used
Pt >40
Obese
Strong genetic connections
No HLA
Mild to moderate glucose intolerance 
Low insulin sensitivity 
Rare ketoacidosis
β cell # variable w/ amyloid deposits 
Variable insulin levels 
Classic symptoms occur sometimes 
Islet amyloid deposits
171
Q

Diabetic Ketoacidosis
Which DM
What precipitates it?
PathoPhys

A

DM1
Usually due to ↑insulin requirement from ↑ stress (infection)
Excess fat breakdown and ↑ ketogenesis from ↑ free fatty acids which are then made into ketone bodies (β hydroxybutyrate > acetoacetate)

172
Q

DKA
Signs and Symptoms
Labs

A

Kussmaul Respirations, nausea, vomiting, abdominal pain psychosis/delirium, dehydration, fruity breath odor (acetone)
Hyperglycemia, ↑H+, ↓Bicarb (aniongap metabolic acidosis), ↑ blood ketone levels, leukocytosis, HyperK (but depleted intracellular K)

173
Q

DKA
Complications
Treatment

A

Mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure
IV fluids, IV insulin, K, Glucose

174
Q

Carcinoid Syndrome
Most common tumor of which organ?
Rule of 1/3
Lab findings

A

Appendix
1/3 metastasize, 1/3 malignant, 1/3 multiple
5-HIAA in urine and niacin deficiency

175
Q

MEN1
Name
Location of tumors
Common presentation

A

Wermer’s Syndrome
“Diamond”
Pituitary (Prolactin, GH)
Parathyroid
Pancreas (Zollinger Ellison, Insulinomas, VIPomas, Glucagonomas)
Commonly presents with kidney stones and stomach ulcers

176
Q

MEN2A
Name
Location of tumors

A

Sipple’s Syndrome
“Square”
Parathyroid and Pheochromocytomas
Medullary thyroid carcinomas (calcitonin)

177
Q

MEN2B

A

“Triangle”
Oral/intestinal ganglioneuromatosis (associated with marfanoid habitus)
Pheochromocytoma
Medullary thyroid carcinomas (calcitonin)

178
Q

Genetics of MEN syndromes

A

Autosomal dominant

2A and 2B associated with ret gene mutation

179
Q

Treatment for DM1

A

Low sugar diet + insulin replacement

180
Q

Treatment for DM2

A

dietary modification, exercise for wt loss, oral hypoglycemics, insulin replacement

181
Q

Insulin Replacement Drugs

A 
Lispro (rapid)
Aspart (rapid)
Glulisine (rapid)
Regular (short)
NPH (intermediate)
Glargine (long)
Detemir (long)
182
Q

Uses of insulin replacement drugs

A

DM1 and DM2, gestational diabetes, hyperK, stress-induced hyperglycemia

183
Q

Toxicity of insulin replacement drugs?

A

Hypoglycemia, Hypersensitivity rxn

184
Q 
Biguanides 
Names
MoA
Uses
Tox
Contraindications
A

Metformin
↓ gluconeogensis, ↑ glycolysis, ↑ peripheral glucose uptake (insulin sensitivity)
First line DM2. Can be used in pts without islet function
GI upset, lactic acidosis
Contraindicated in renal failure

185
Q

First generation sulfonylureas

A

Tolbutamide, Chlorpropamide

186
Q

Second generation sulfonylureas

A

Glyburide, Glimepiride, Glipizide

187
Q

Sulfonylureas
MoA
Use
Tox

A

Close K channels in β cells –> insulin release
DM2. Requires some islet function (useless in DM1)
1st gen: disulfiram-like effects
2nd gen: hypoglycemia

188
Q 
Glitazones/Thiazolidinediones
Names
MoA
Use
Tox
A

Pioglitazone, Rosiglitazone
↑ insulin sensitivity in peripheral tissue. Binds PPARγ nuclear receptor
DM2
Wt gain, edema, Hepatotoxic, heart failure

189
Q 
α glucosidase inhibitors 
Names
MoA
Use
Tox
A

Acarbose, Miglitol
Inhibits intestinal brush border α glucosidase
Delayed sugar hydrolysis and glucose absorption
DM2
GI disturbances

190
Q 
Amylin analogs
Names
MoA
Use
Tox
A

Pramlintide
↓ glucagon
DM 1 and 2
Hypoglycemia, nausea, diarrhea

191
Q 
GLP1 analog 
Names
MoA
Use
Tox
A

Exenatide, Liraglutide
↑ insulin, ↓ glucagon
DM2
Nausea, vomiting, diarrhea

192
Q 
DPP4 inhibitors 
Names
MoA
Use
Tox
A

Linagliptin, Saxagliptin, Sitagliptin
↑ insulin, ↓ glucagon
DM2
Mild urinary and respiratory infections

193
Q

Levothyroxine, Triiodothyronine
MoA
Use
Tox

A

Thyroxine replacement
Hypothyroidism, myxedema
Tachycardia, heat intolerance, tremors, arrhythmias

194
Q

Use of GH as a medicine

A

GH deficiency and Turners Syndrome

195
Q

Uses of octreotide

A

Acromegaly, Carcinoid, Gastrinoma, Glucagonoma, Esophageal varices

196
Q

Uses of Oxytocin

A

Stimulates labor, uterine contraction, milk let-down. Controls uterine hemorrhage

197
Q

Uses of Desmopressin

A

Central DI

198
Q 
Demeclocycline 
Class of drugs 
MoA
Use
Tox
A

Tetracycline
ADH antagonist
SIADH
Nephrogenic DI, Photosensitivity, abnormalities or bone and teeth

199
Q 
Glucocorticoids
Names
MoA
Use
Tox
A

Hydrocortisone, Prednisone, Triamcinolone, Dexamethasone, Beclomethasone
↓ production of leukotrienes and prostaglandins by inhibiting PLA2 and expression of COX2
Addison’s disease, Inflammation, Immune suppression, Asthma
Cushing’s syndrome, Peptic ulcers, Adrenocortical atrophy.
Adrenal insufficiency if stopped abruptly

USMLE STEP 1 (25 decks)

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