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Boards High Yield > Endo > Flashcards

Endo Flashcards

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

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