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Flashcards in Final Deck (129):
1

physiological causes of hyperprolactinoemia

pregnancy
breastfeeding

2

pharmacological causes of hyperprolactinoemia

estrogen
dopamine receptor antagonist, antidepressants

3

pathological causes of hyperprolactinoemia

1. Prolactinoma
2. Hypothyroidism
3. Renal Failure
4. Stalk Effect (pressure)

4

female presents with:
1. Galactorrhea
2. Loss of libido
3. Amenorrhea (25%)
4. Infertility

hyperprolactinomeia

*Microprolactinoma (less than a cm)

5

male presents with:
1. Gynecomastia
2. Loss of libido
3. Erectile Dysfunction
4. Infertility

hyperprolactinomeia

*Macroprolactinoma (larger than a cm, can also cause pressure related problems)

6

Insulin tolerance test: gold standard, induced hypoglycemia

GH

7

how do you screen for GH deficiency

ICFI level (less variable than GH)

8

what is clonidine suppose to do

inhibit somatastatin

9

presents with:
-Causes include tumors and familial forms
-Abnormally short height in childhood, but is well proportioned
-associated with physical defects: cleft lip/plate

pituitary dwarfism

*due to deficiency in GH

10

treatment of pituitary dwarfism

GH injection

11

how do you screen for GH excess

IGF-I

*failure to suppress-75 OGTT

12

presents with:
-increase in body size/height
-disproportionately long arms and legs
-causes problems to heart and CV system

Gigantism
(Before growth plates close)


*GH excess

13

Gigantism is associated w/ what other abnormality

problems with heart and CV system

14

presents with:
-Enlarged hands, feet, jaw, brow bone
-Separation of teeth****
-Abnormal glucose tolerance, arthritis, heart failure

Acromegaly
(in adults after epiphyseal plates close)

*GH excess

15

how do you test for acromegaly

-No change really in GH (decrease over time though)
-Elevated IGF-I
-75g oral glucose load

16

presents with:
-Polyuria: production of large amount of dusted urine
-olydipsia: excess drinking

ADH/vasopressin deficiency

17

how does ADH/vasopressin deficiency occur

damage to hypothalamus

18

how do you diagnose ADH/vasopressin deficiency

water deprivation with administration of exogenous ADH

19

in adults is usually damage to the pituitary gland or hypothalamus, most commonly due to surgery, a tumor, an illness (such as meningitis), inflammation or a head injury. For children, the cause is often an inherited genetic disorder. In some cases the cause is unknown. This damage disrupts the normal production, storage and release of ADH.

central diabetes insipidus

*corrects with exogenous

*ADH/vasopressin deficiency

20

occurs when there's a defect in the kidney tubules — the structures in your kidneys that cause water to be excreted or reabsorbed. This defect makes your kidneys unable to properly respond to ADH. The defect may be due to an inherited (genetic) disorder or a chronic kidney disorder. Certain drugs, such as lithium and demeclocycline (a tetracycline antibiotic), also can causes it

nephrogenic diabetes inspidus

*renal resistance

*ADH/vasopressin deficiency

21

what causes *ADH/vasopressin excess

head injury, meningitis, tumor (lung carcinomas: ectopic production; rarely originates from the posterior pituitary), Drugs

22

presents with:
hyponatremia,
hyperosmolar urine,
cerebral edema

syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

**ADH/vasopressin excess

23

how do you diagnose syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

water load test
-20mL water/kg (1500 mL max)
-See if concentration changes: Urine collected is still hyperosmolar (fails to suppress)

24

Anterior pituitary hypo function from any etiology leads to

Simmond’s Disease

25

presents with:
1. Central Obesity (most common feature, “moon facies”, “buffalo hump”)
2. Thin skin —> striae (subtle)
3. Hirsutism
4. Hypertension
5. Hyperglycemia
6. Osteoporosis
7. Immunosuppression

Cushing syndrome

*glucocorticoid excess

26

how to diagnose Cushing syndrome

a. Step 1: Establish hypercortisolism
i. 24 hour urine free cortisol (cushing syndrome will have a lot in the urine)
ii. 1 mg dexamethasone test (give them at 8am, you would expect it to go down if normal (suppression), with cushing’s it doesn’t do that, no negative feedback)
b. Step 2: determine if hypercortisolism is ACTH-dependent or ACTH-independent
c. Step 3: Localize tumor

27

-Hypersecretion of ACTH from pituitary
-Small cell carcinoma of the lung, bronchial carcinoid, medulla thyroid cancer, pheochromocytoma)
-May be suppressed by exogenous dexamethasone

secondary Cushing syndrome

*Glucocorticoid Excess

28

-Adrenal cortical hyperplasia-rare
-Adrenal cortical adenoma/carcinoma
-ACTH low, Adrenal cortical atrophy, cannot be suppressed by exogenous dexamethasone

primary cause Cushing syndrome

*Glucocorticoid Excess

29

-exogenous corticosteroid medication
-most common cause, adrenal cortical atrophy, ACTH low

iatrogenic cause of cushing syndrome

*Glucocorticoid Excess

30

presents with:
Hypertension, Sodium and water retention, Hypokalemia

Hyperaldosteronism (Conn Syndrome)

31

how to diagnose Hyperaldosteronism (Conn Syndrome)

-primary: decrease serum renin
-Secondary: increased serum renin

32

causes of Hyperaldosteronism (Conn Syndrome)

-Secondary: Renal Ischemia, Renal Tumors, Edema (cirrhosis, nephrotic syndrome, cardiac failure), Pregnancy
-Primary: adrenal cortical tumor

33

presents with:
adrenal based virilization, Masculization of females (ambiguous genitalia at birth, precocious pubic hair, clitoromegaly), Precocious puberty in males

congenital adrenal hyperplasia

34

how to diagnose congenital adrenal hyperplasia

Decreased cortisol,
increased ACTH,
increased 17a-hydroxyprogesterone

35

causes of congenital adrenal hyperplasia

1. Carcinoma or adenoma
2. Congenital enzyme defect
-21-hydroxylase deficiency most common
-leads to diminished cortisol production
-compensation is increased ACTH
-Results in adrenal hyperplasia and increase sex steroids

36

Chronic insufficient cortisol and usually aldosterone

Addison's disease

37

presents with:
1. Anorexia, weight loss, vomiting
2. Weakness and lethargy
3. Hypotension
4. Hyponatremia and hyperkalemia
5. Chronic dehydration
6. Increased pigmentation of skin: Due to MSH, found in nearly all patients

Addison's disease

*Chronic insufficient cortisol and usually aldosterone

38

how to diagnose Chronic insufficient cortisol and usually aldosterone

-If cortisol doesn’t follow normal pattern (lower baseline) and no fluctuation like normally expected)
-if we gave ACTH, we would expect cortisol to go up, but it doesn’t (primary disease)
-if we gave ACTH and have secondary disease would spike up like “normal” because adrenal glands are fine

39

Waterhouse-Friderichson syndrome

acute adrenal insufficiency

40

i. Hemorrhagic necrosis of the adrenal cortex
ii. Associated with disseminated intravascular
iii. can be associated with Neisseria meningitidis sepsis

Waterhouse-Friderichson syndrome

*acute adrenal insufficiency

41

presents with:
**without prompt hormone replacement —> death
1. Intractable vomiting
2. abdominal pain
3. salt and water loss with hypovolemic shock
4. Failure of gluconeogenesis resulting in hypoglycemia

Waterhouse-Friderichson syndrome

*acute adrenal insufficiency

42

Tumor derived from chromaffin cells

pheochromocytoma

43

presents with:
1. Hypertension (episodic or sustained): surgically correctable (younger hypertensive patients)
2. headaches
3. tachycardia
4. sweating and nervousness
5. potential hyperglycemia
6. pallor
7. tremor

pheochromocytoma

44

how to diagnose pheochromocytoma

increased plasma levels or 24 hour urinary excretion of catecholamine and Metanephrines (metabolites)

45

presents with:
1. children (usually less than 3 years old)
2. presents as a large abdominal mass
3. 60% have metastatic disease, most commonly involving bone

neuroblastoma

46

test results:
1. Defective synthesis of catecholamines —> accumulation and excretion of intermediates Vanillylmandelic acid (VMA), homovanillic acid (HVA), and dopamine
2. diagnosis: elevated urinary HVA and VMA
3. Microscopic: Rosettes (own developed structure)

neuroblastoma

47

in primary thyroid function abnormalities what would the test results look like for:
hyperthyroidism
hypothyroidism
hyperparathyroidism

Primary- issue with thyroid gland itself
-Hyperthyroidism: low TSH
-Hypothyroid: high TSH
-Hyperparathyroidism: high PTH, high Ca2+

48

in secondary thyroid function abnormalities what would the test results look like for:
hyperthyroidism
hypothyroidism
hyperparathyroidism

Secondary- issue with pituitary
-Hyperthyroidism: high TSH
-Hypothyroidism: low TSH
-Hyperparathyroidism: high PTH, normal Ca2+

49

labs for primary and secondary hyperthyroidism

primary: low TSH,
Secondary: high TSH

50

causes of hyperthyroidism

1. Pregnancy increases TBG (increases the total amount and normal free amount so normothyroid)
2. Hyperplasia/goiter (85%)
3. Iatrogenic (exogenous hormone)
4. Adenoma (thyroid or pituitary)
5. Thyroiditis
6. Ectopic- struma ovarii produces T4/T3

51

presents with:
Palpitations, tachycardia, weakness, weight loss, diarrhea, heat intolerance, hyperhydrosis, menstrual changes, fine tremor, hyper-reflexes

hyperthyroidism

52

labs for primary and secondary hypothyroidism

primary: TSH high,
Secondary: TSH low

53

causes of hypothyroidism

1. Damage to pituitary/hypothalamus
2. Damage to thyroid (surgery, radiation)
3. Congenital
4. Iodine deficiency
5. Iatrogenic (lithium Rx)
6. Thyroiditis
a. DeQuervian thyroiditis (Giant Cell Thyroiditis)

54

presents with:
1. Physically and mentally slow (confused with depression), cold intolerant, hypohydrosis, constipation, weight gain, menorrhagia, generalized myxedema, non-pitting edema

hypothyroidism

55

labs for primary and secondary hyperparathyroidism

Primary: high PTH (autonomous), high Ca2+
Secondary: high PTH (appropriate), normal Ca2+

56

causes of hyperparathyroidism

1. Adenoma (80%)
2. Hyperplasia (15%)
3. Carcinoma (5%)

57

presents with:
Bone pain 2’ to fractures, nepthrolithiasis, constipation, lethargy, weakness, valvular calcifications
-renal failure

hyperparathyroidism

*Secondary hyperparathyroidism causes renal failure (most common cause) and leads to hyperplasia of all glands

58

presents with:
Tetany, paresthesia, mental status changes (seizures), cardiac arrhythmia

hypoparathyroidism

59

causes of hypoparathyroidism

1. Iatrogenic damage to parathyroid (surgery, radiation)
2. Congenital (DiGeorge Sydnrome)
3. Idiopathic (autoimmune?)

60

labs of hypoparathyroidism

low PTH with low serum Ca2+

61

presents with:
painless goiter, exophthalmos (bulging eyes due to build up of scar tissue behind the eyes), pretibial myxedema

graves disease

- thyroid hyperplasia
*more common in females

62

pathogenesis:
1. Autoimmune production of antibodies which bind to and stimulate TSH receptors (TSI)
2. Moleular mimicry: Yersinia enterocolitica, some retroviruses
3. HLA: induction of class II expression, HLA-DRB1*08 and DRB3*0202 associated, DRB1*07 protective

graves disease

63

Histology:
1. Hyperplastic infoldings of the follicular cells
2. Clear vacuoles

graves disease

64

presents with:
painless, diffuse enlargement
more common in middle aged women

Hashimotos (lymphocytic) thyroiditis

65

pathogenesis:
1. Autoimmune
a. Anti-TPO(thyroid peroxidase) and/or anti-Tg (thyroglobulin)
b. Anti-TSHR that blocks receptor activity
2. Slow destruction of thyroid tissue ultimately leading to hypothyroidism

Hashimotos (lymphocytic) thyroiditis

66

histology:
lymphocytic inflammation

Hashimotos (lymphocytic) thyroiditis

67

presents with:
-Absence of normal thyroid tissue
-Abnormalities of many neck structures (thymus, thyroid, parathyroid, aortic arch)

DiGeorge Sydrome

68

-TH necessary for normal brain development
-In utero due to maternal hypothyroidism
-Neonatal due to baby’s hypothryoidism
-presents with developmental delay

Cretinism

69

-Diffuse enlargement
-Iodine deficiency
-Ex. Graves Disease (sign/symptoms of hyperthyroidism, painless goiter, exophthalmos)

simple goiter

70

presents with:
1. Multiple episodes of hyperplasia and involution
2. Usually asymmetric
3. Pressure on the throat/airway: Trouble breathing/swallowing, wheezing, coughing, a choking feeling
4. can be confused with carcinoma

multinodular goiter- irregular growth

71

List the changes in laboratory results associated with nonthyroidal illness, especially the results that correlate with increased mortality.

-Also called euthyroid sick syndrome

c. TSH: Normal
d. Free T4: Low to Normal
e. Free Reverse T3: High
f. Total T3: Low
g. Total T4: Low

*Mortality 50% when serum free T4 is less than 4 ug/dL and 80% when less than 2 ug/dL

72

-Psammoma bodies (calcifications, can be seen in U/S study), clear or grooved nuclei, nuclear pseudoinculsions (nuclear features is how this is diagnosed)

papillary primary thyroid carcinoma

*most common 80-90%

73

prognosis of papillary primary thyroid carcinoma

excellent bc its slow growing

*most common in 20-40y.o

74

papillary primary thyroid carcinoma tends to have metastasis where

lymph node

75

-Impossible to diagnose with biopsy (cells themselves do not have the same nuclear changes as papillary carcinoma)
-capsular invasion and invasion into a blood vessel (what looking for to distinguish from benign adenoma)

follicular primary thyroid carcinoma

*15%

most common in 40-50 y/o

76

follicular primary thyroid carcinoma tends to have metastasis where

hematogensous

77

80% sporadic/20% part of multiple endocrine neoplasia

medullary primary thyroid carcinoma

78

prognosis of follicular primary thyroid carcinoma

good prognosis

79

presents as:
-Most common in 40-60 y/o sporadic, or 30-40y/o for MEN patients
-Secrete calcitonin → amyloid
-Inhibits renal and GI absorption as well as bone resorption so may have signs/symptoms of hypocalcemia
-Use calcitonin stain (IHC)

medullary primary thyroid carcinoma

80

prognosis of medullary primary thyroid carcinoma

fair (requires thyroid removal)

81

histology:
No colloid, more solid sheet of tumor cells, Amyloid (big pink structure)

medullary primary thyroid carcinoma

82

-Undifferentiated, or de-differentiation of another type of thyroid carcinoma
2. > 60 y/o

Anaplastic Thyroid Carcinoma (Very rare,

83

prognosis of Anaplastic Thyroid Carcinoma

horrible Prognosis (survival

84

Hard to diagnosis under the microscope, sometimes will lose markers that you would stain for thyroid to determine cancer, but can lose those (may not even look like thyroid cells anymore)

Anaplastic Thyroid Carcinoma

85

Familial propensity for hyperplasia and/or neoplasia of endocrine organs

MENI and MENII

86

3 P's of MENI

Parathryoid hyperplasia, pancreas tumors, pituitary adenoma

87

gene (Chr 11), tumor suppressor, AD

MENI

88

RET proto-oncogene (Chr 10), AD

MENII A/B

89

what is associated with MENII

Medullary thyroid carcinoma,
adrenal pheochromocytoma,
parathyroid hyperplasia

90

etiologies of acute pancreatitis

1. duct obstructions
2. acinar cell injury
3. defective intracellular transport

91

cholelithiasis/gallstones, tumor, ampulllary obstruction, chronic alcoholism, ductal concretions
leads to

acute pacreatitis from duct obstruction

92

alcohol, drugs, trauma, hypertriglyceridemia (>100mg/dL) →ischemia, viruses, hypercalcemia→ duct deposition, trypsinogen activation, parasites pancreas divisum)
leads to

acute pancreatitis from acinar cell injury

93

Metabolic injury- experimental, alcohol, duct obstruction
leads to

acute pancreatitis from defective intracellular transport

94

CT findings of acute pancreaitis

-Diffusely ENLARGED PANCREAS with low density from EDEMA
-Density of pancreas is loess than liver and spleen with IV contrast
-Pancreas is wider than abdominal aorta diameter indicating that it has increased in size

95

Histology:
-Neutrophil and lymphocyte infiltrate
-Necrosis
-Pseudocyst formation or pancreatic abscess

acute pancreatitis

96

labs with acute pancreaitits

-elevation of pancreatic enzymes (amylase- not as specfic, lipase*)
-Potential hypocalcemia depending on degree of fat necrosis
-Severity related to systemic release of digestive enzymes (elevated WBC, DIC, ARDS, systemic fat necrosis, shock)

97

complications associated with acute pancreaitis

1. Interstitial inflammation and edema
2. Proteolysis (proteases)
3. Fat necrosis (lipase, phospholipases)
4. Hemorrhage of splenic artery or vein (elastase)

98

presents with:
back or abdominal pain (epigastric), fever, tachycardia, shallow respirations

acute pancreatitis

99

Irreversible destruction with fibrosis

chronic pancreatitis

100

etiologies of chronic pancreatitis

1. Alcohol abuse
2. Cystic fibrosis
3. Pancreas divisum
4. Pseudocyst
5. Calculi
6. Concretions
7. Hereditary (ie. PRRS1- cannot turn of trypsin, SPINK1-can’t inhibit pancreatic enzymes, CFTR mutations)

101

-Localized collection of fluid and necrotic material lined by fibrous tissue
-Fluid with high concentration of pancreatic enzymes
-True cysts are lined by epithelial tissue, this is just scar tissue

pseudocyst

*associated with chronic pancreatitis

102

Histology:
-fibrosis
-Reduce numbers and size of acini
-eventual loss of islets

chronic pancreatitis

103

CT findings for chronic pancreatitis

a. Dystrophic calcifications
b. Dilated pancreatic duct

104

labs for chronic pancreatitis

+/- amylase or lipase elevation

105

complications associated with chronic pancreatitis

1. Jaundice
2. Persistent or recurrent abdominal or back pain
3. Malabsorption
4. DM
5. +/- amylase or lipase elevations

106

-Arise from acinar and ductal cells
-Show up in head of pancreas- compress the common bile duct

exocrine pancreatic tumors

107

risk factors for exocrine pancreatic tumors

Cigarette smoking, chronic pancreatitis, DM

108

presents with:
Painless jaundice***
weight loss,
DM

exocrine pancreatic tumors

109

-Arise from islet cells
-Rare, often small tumors

endocrine pancreatic tumors

110

presents with:
1. Due to hypersecretion of pancreatic hormones
2. Insulinoma: hypoglycemia
3. Glucagonoma: hyperglycemia (presents as DM)
4. Gastrinoma: gastric acid secretion, multiple gastric ulcers, duodenal ulcers

endocrine pancreatic tumors

111

etiology of type 1 DM

-Absolute deficiency of insulin production
-Autoimmune destruction of B islet cells of the pancreas

*Need to lose >90% islet less
-Onset in childhood

112

etiology of type 2 DM

-due to lack of response by tissue to insulin without a compensatory increase in insulin secretion (relative insulin deficiency)

*Insulin resistance

113

ii. Reduced signal transduction from cell surface receptors for insulin
iii. Metabolic changes caused by obesity (increased FA, inflammation, adipokines)

type 2 DM

114

familial association of type 2 DM

-Onset in adulthood
-Possible slowing or reversal with lifestyle changes
-Can result in “Islet burn out- amyloid deposition in islets ”→ IAPP (islet amyloid polypeptide, and become insulin dependent

115

Can result in “Islet burn out- amyloid deposition in islets ”→ IAPP (islet amyloid polypeptide, and become insulin dependent

type 2 DM

116

gestational DM is due to

-Diabetes during pregnancy
-Due to hPL + predisposition
-Overt DM

117

secondary causes of DM

-Recognized genetic defects (hemochromatosis, CF, insulin receptor mutations)
-Exocrine pancreatic defect (pancreatitis)
-Other endocrinopathies (Cushings, acromegaly)
-Drugs
-Infections

118

diagnostic criteria for DM

-Random plasma glucose >200mg/dL (11.1 mmol/L), with symptoms
-Fasting plasma glucose > 126mg/dL (7 mmol/L)
-Abnormal oral glucose tolerance test

*Hemoglobin A1c > 6.5% (avg glucose over several months)

-Best if results are confirmed by repeating testing

119

how to diagnose gestational DM

-Fasting plasma glucose ≥92 mg/dL ,

120

complications associated with DM

-glycosylation
-polyol pathway
-Thickening of smaller arteries due to hyaline depositions and smooth muscle proliferation
-accelerated atherosclerosis
-increased risk of infection
-risk of LGA infant

121

thickening of smaller arteries due to hyaline depositions and smooth muscle proliferation in DM:
Retinopathy-->
Nephropathy -->
Peripheral neuropathy -->
Autonomic neuropathy -->

Retinopathy--> blindness
Nephropathy --> renal failure
Peripheral neuropathy --> sensory and motor loss
Autonomic neuropathy --> abnormal bowel, bladder function

122

pathogenesis:
Glucose non-enzymatically attaches itself to the N-terminal end of proteins
-The more glucose you have around, the more that attaches to proteins

glycosylation

123

-Bind to RAGE on endothelial cells promoting inflammation, generation of reactive oxygen species, proliferation of vascular smooth muscle
-Results in neuropathy

glycosylation

124

Most of the long-term complications of DM are due to

protein glycosylation

125

-Cell that do not need insulin for glucose transport (nerves, lens, kidney, blood vessels)
-Marked increase in aldose reductase (AR) activity and the accumulation of sorbitol
-Normal:

polyol pathway

126

-Less antioxidant activity of glutathione reductase pathway→ results in cell damage
-Osmotic: sorbitol accumulation in tissues causes osmotic swelling and cell damage
-NADPH supply: low NADPH compromises the ability of the cell to protect itself from oxidative stress

polyol pathway

127

Less antioxidant activity of glutathione reductase pathway→ results in __

cell damage

128

Osmotic: sorbitol accumulation in tissues causes

osmotic swelling and cell damage

129

NADPH supply: low NADPH compromises the ability of the cell to

protect itself from oxidative stress