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PAS 531 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Metabolic syndrome

A

People at high risk of diabetes and cardiovascular disease

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2
Q

Metabolic syndrome associated condition

A

Small dense LDL
Proinflammatory state
Hyperinsulinemia
Hyperuricemia
Chronic kidney disease
Dementia/cognitive decline
Steatosis, fibrosis, cirrhosis
Insulin resistance
PCOS
Sleep apnea

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3
Q

Metabolic syndrome labs and tests to consider

A

Hemoglobin A1C
Lipid panel
BMP
C-reactive protein
Liver panel
TSH
Uric acid
ECG
Vascular ultrasound
Stress test
Sleep study

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4
Q

Underweight BMI

A

<18.5

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5
Q

Normal BMI

A

18.5-24.9

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6
Q

Overweight BMI

A

25-29.9

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7
Q

Obesity class 1

A

30-34.9

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8
Q

Obesity class 2

A

35-39.9

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9
Q

Extreme obesity (class 3)

A

> 40

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10
Q

Man waist size at risk of obesity

A

> 40

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11
Q

Woman waist size at risk of obesity

A

> 35

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12
Q

Man waist to hip ratio at risk of obesity

A

> 1

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13
Q

Woman waist to hip ratio at risk of obesity

A

> 0.85

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14
Q

Leptin

A

Tells brain you’re full
Decrease when you’re fat

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15
Q

Grhelin

A

Tells you you’re hungry

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16
Q

BMI indications for weight loss meds

A

> 27 with comorbidities
30

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17
Q

Phentermine

A

Weight loss drug
Adrenergic agonist
Decrease appetite
Short term use

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18
Q

Orlistat

A

Weight loss drug
Inhibits intestinal lipase
Causes diarrhea if eat lots of fat

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19
Q

Phentermine/topiramate

A

Weight loss drug
GABA modulation
Decreases appetitie and speeds metabolism
TERATOGENIC

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20
Q

Naltrexonebupropion

A

Weight loss drug
Appetite suppression
Two tabs twice daily over four weeks

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21
Q

Liraglutide

A

Weight loss drug
GLP-1 receptor agonist
Increases satiety
Daily injectable

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22
Q

Semaglutide

A

Weight loss drug
GLP-1 receptor agonist
INcreases satiety
Weekly injectable
Contraindicated for pts with pancreatitis or thyroid C-cell tumor hx

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23
Q

Tirzepatide

A

Weight loss drug
Dual GLP-1 agonist and GIP
ONce weekly subcutaneous injection
Fasting ansd post-prandial glucose
Lowers A1C by more than 2%

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24
Q

Common adverse effects of GLP-1 receptor agonist

A

Nausea
Vomiting
Diarrhea
Constipation

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25
Q

Less common more serious adverse effects of GLP-1 receptor agonist

A

Pancreatitis
Intestinal obstruction
Gastropareisis
Medullary thyroid carcinoma

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26
Q

Orbera

A

Intragstric balloon placed and removed endoscopially

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27
Q

Obalon

A

Intragastric balloon swallowed then inflated then removed endoscopally

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28
Q

Transpyloric shuttle

A

Removable gastric balloon blocks pylorus so food sits in stomach longer and you feel fuller
Removed by endoscopy

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29
Q

Duodenal jejunal bypass liner

A

Impermeable sleeve
Only approved for one year of use

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30
Q

Aspire Assist Aspiration Device

A

Endoscopically placed tuvbe to aspirate food after meals

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31
Q

Super absorbent hydrogel capsules

A

Take three capsules before two big meals of day

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32
Q

Laprascopic adjustable gastric band

A

Silicone band placed around upper part of stomach
Adjustable and reversible.
Slower weight loss
Lesss overall weight loss

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33
Q

Laparascopic sleeve gastrectomy

A

Small sleeve-shaped stomach is created
Outpatient
Bad for pts with reflux

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34
Q

Endoscopic sleeve gastroplasty

A

70-80% of stomach is collapsed with sutures
Reversible if necessary
Outpatient

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35
Q

Roux-en-Y Gastric Bypass

A

Small intestine attached to esophagus
Stomach reattached down stream so you can still have intrinsic factor.
Can cause malabsorption
Can CURE DIABETES

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36
Q

What is a cure for diabetes

A

Roux-en-Y Gastric Bypass

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37
Q

Biliopancreatic diversion with duodenal switch

A

Malabsorptive process
Stomach is made smaller
Small inestine is bypassed
Need vitamin supplementation (B12)

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38
Q

Chief cells

A

On parathyroid
Secrete parathyroid hormone

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39
Q

Parathyroid hormone

A

Secreted by Chief cells
Stimulates osteoclast activity to pull Ca from bone into blood

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40
Q

Parathyroid hormone effects on kidney

A

Allows DCT to be more permeable to Ca so it is Reabsorbed raising blood Ca levels

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41
Q

Parathyroid effect on GI

A

Turns Vitamin D into active form
Causes calcium channels in gut to be expressed
Allows more calcium from GI tract to be absorbed into blood

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42
Q

Calcitonin

A

Comes from thyroid gland
Inhibits osteoclast activity thus increasing osteoblast activity

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43
Q

Two most common causes of hypercalcemia

A

Primary hyperparathyroidism
Malignancy

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44
Q

Non-parathyroid mediated hypercalcemia causes

A

Vitamin D intoxication
High bone turnover
Multiple endocrine neoplasia
Renal failure
Hyperthyroidims
Acromegaly
Pheochromcytoma
Adrenal insufficiency

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45
Q

Medications that cause hypercalcemia

A

Thiazide diuretics
Lithium
Excessice vitamin A

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46
Q

Hypercalcemia symptoms

A

Bone disease (bones)
Nephrolithiasis (stones)
Abdominal pain (groans)
AMS (psychiatric moans)

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47
Q

Bone disease

A

Osteitis fiibrosa cystica
Decreased bone mineral density
INcreased risk of fractures

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48
Q

What do you have to relate your calcium labs to for each pt if abnormal

A

Albumin
Low albumin makes hypercalcemia severity underestimated
High albumin makes calcium level look high even when its not (pseudohypercalcemia)

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49
Q

Hypercalcemia affect on EKG

A

Short QT interval

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50
Q

Hypercalcemia cardiac problems

A

HTN
Vascular calcification
Left ventricular hypertrophy
Short QT
Arrythmias

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51
Q

Moderate hypercalcemia treatment

A

Saline hydration
Bisphosphonates

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52
Q

Bisphosphonates

A

-nate and zoledronic acid
Used against osteoclast mediated bone loss
Used for osteoporosis, paget disease, metastatic bone disease, and hypercalcemia

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53
Q

Most common presentation of hypercalcemia

A

Asymptomatic

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54
Q

Severe hypercalcemia treatment

A

IV isotonic saline
Subcutaneous calcitonin
IV bisphosphonate
Dialysis is last resort

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55
Q

Primary hyperparathyroidism

A

Abnormal regualtion of parathyroid hormone secretion

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56
Q

Parathyroid adenoma

A

Most common cause of primary hyperparathyroidism
Tumor made of chief cells
Can be on parathyroid or ectopic lotcation

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57
Q

Causes of primary hyperparathyroidism

A

Parathyroid adenoma
Glandular hyperplasia
Carcinoma
Radiation
Low calcium intake (parathyroid overstimulated)
Genetics
Meds

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58
Q

How do thiazide diuretics cause hypercalcemia

A

Less urinary calcium is excreted

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59
Q

Releationship between phosphate and calcium

A

Inverse

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60
Q

Relationship between alkaline phosphatase and calcium

A

direct

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61
Q

Hyperparathyroid diagnostics

A

Technetium sestamibi scan
Checks for adenomas

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62
Q

Treatment of primary hyperparathyroid asymptomatic patient

A

Monitor
Stop meds associated with hyperparathyroidism
Hydration

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63
Q

Treatment of primary hyperparthyroid symptomatic patient

A

Surgical excision of abnormal tissue
Loop diuretics
Hydration
Calcimimetics
Bisphosphonates

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64
Q

Loop diuretics job against primary hyperparathyroidism

A

Inhibits sodium and calcium reabsorption

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65
Q

Calcimimetics job against primary hyperparathyroidism

A

Activates calcium sensing receptors so parathyroid doesn’t release PTH

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66
Q

What is a person given after parathyroid surgery

A

Calcium and Vitamin D supplementation

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67
Q

Secondary hyperparathyroidism

A

Calcium is low!!!! causing prathyroid gland to be overstimulated
Disease outside parathyroid gland causes gland to become hyperactive.
Parathyroid gland itself is not diseased

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68
Q

Causes of secondary hyperparathyroidism

A

Renal failure
Malabsorption (celiac and chrohn)
Vitamin D deficiency

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69
Q

Secondary hyperparatyroidism Symptoms

A

Asymptomatic

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70
Q

Secondary hyperparathyroidism diagnosis

A

Low calcium
High PTH
Order studies to check renal function (GFR, BUN, creatinine)
Vitamin D deficiency

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71
Q

Treatment of renal failure

A

supplememntation with calcium and vitamin D
Medications that activate Ca receptors (calcimimetics)

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72
Q

Phosphate binders

A

Prevent body from absorbing phosphate in food.
Used to treat secondary hyperparathyroid

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73
Q

Hypocalcemia causes

A

Renal failure
Hypoparathyroidism
Vitamin D deficiency
Hypomagnesemia
Loop diuretics
Foscarnet
Burns

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74
Q

Hypocalcemia symptoms

A

Trousseau sign
Cvostek sign
Convulsions
Arrhythmia
Tetany
Spasms and stridor
Numbess in fingers

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75
Q

Hypocalcemia EKG problems

A

Prolonged QT

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76
Q

Treatment for hypocalcemia

A

IV calcium gluconate
PO calcium

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77
Q

Hypoparathyroidism causes

A

Usually post-surgery
Destruction of parathyroid glands
Abnormal parathyroid gland development
Altered regulation of PTH production
Impaired PTH actoin
Autoimmne
Mg defciency
Iron overload
Copper overload

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78
Q

What happens when PTH secretion is insufficient

A

Hypocalcemia

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79
Q

How is cortisol released

A

CRH from hypothalamus causes ACTH to be released from ant pit
ACTH causes cortisol to be released from adrenal gland

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80
Q

Cushing syndrome

A

High cortisol
Neoplasia increases production of cortisol
ACTH dependent (90%)
ACTH independent (10%)

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81
Q

Addison’s disease

A

Low cortisol
Destruction of adrenal gland or inherited autoimmune disorder disrupts cortisol synthesis

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82
Q

Where is cortisol produced

A

Zona fasciculata and zona reticularis of adrenal cortex

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83
Q

Cortisol characteristics

A

Glucocorticoid
Secreted unbound
Circulates bound to plasma proteins
Only 4% is free for use
Excreted in urine and stool

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84
Q

When is cortisol highest

A

Morning

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85
Q

ACTH dependent cushing syndrome cause

A

ACTH-secreting pituitary tumor (cushing’s disease)
Pituitary adenoma (cushing’s disease)
Small cell lung carcinoma
Medullary thyroid carcinoma
Carcinoid tumors (bronchus)

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86
Q

Carcinoma

A

Malignant tumor

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87
Q

Adenoma

A

benign tumor

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88
Q

ACTH independent cushing syndrome cause

A

Adrenal carcinoma
Adrenal adenoma

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89
Q

Latrogenic cushing syndrome cause

A

HPA axis supprestion
Prolonged steroid use

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90
Q

Pseudo-cushing syndrome

A

conditions biochemically same as cushings
Elevated cortisol
Disruption of cortisol secretion
Depression
Chronic alcoholism
Chronic kidney disease

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91
Q

Common findings in other body systems from cushing syndrome

A

Muscle atrophy
Hyperglycemia
Weight gain from adipose tissue
Insulin resistance
Skin thinning
Striae
Bruising
Osteoporosis
Secondary Hyperparathyroidism
HTN
Susceptibility to infection
Hirstuism and acne
Buffalo hump
Moon face
Apple body

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92
Q

Initial screening for hypercortisolism

A

24 hour urinary free cortisol.
Confirms hypercortisolemia

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93
Q

Dexamethasone suppression test

A

Establishes diagnosis of cushing syndrome

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94
Q

What happens if you give desmethasone to healthy person

A

Cortisol levels drop

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95
Q

What happens if you give dexmetasone to person with cushing syndrome

A

cortisol won’t drop

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96
Q

How to determine if cushing syndrome is ACTH dependent or independent and what to do for each

A

ACTH serum Less than 5 ACTH independent so get adrenal CT
ACTH serum Greater than 20 means ACTH dependent so get pituitary MRI

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97
Q

Primary adrenal insufficiency

A

Addison disease
Dysfunctino of adrenal cortices

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98
Q

Secondary adrenal insufficiency

A

Anterior hypopituitarism
Deficient secretion of ACTH

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99
Q

Acute adrenal crisis

A

Emergency due to insufficient corisol
Abrupt withdrawal of glucocorticoid relacement
PRecipitated by trauma or infection

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100
Q

Most common cause of adrenal insufficiency

A

Autoimmune

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101
Q

Adrenal insufficiency treatment

A

Hydrocortisone
Fluid replacement
Adress underlying cause

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102
Q

Adrenal insufficiency (addison) presentation

A

GI symptoms
Bronze pigmentation
Weakness
Weightloss
HTN

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103
Q

Primary adrenal insufficiency treatment

A

Hydrocortisone
Fludrocortisone

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104
Q

Secondary adrenal insufficiency treatment

A

Hydrocortisone

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105
Q

How can we clinically see aldosterone issues in lab

A

Potassium
High aldosterone looks like HTN with hypokalemia

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106
Q

Aldosterone job

A

Sodium retention (reabsorption) in kidneys causing potassium diuresis and increased urine acidity.

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107
Q

Primary hyperaldosteronism cause

A

Bilateral adrenal hyperplasia
Adrenocortical carcinoma
Adrenocortical adenoma

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108
Q

Secondary hyperaldosteronism cause

A

Renal artery stenosis
Decreased intravascular volume (heart failure, chronic diuretic or laxative use)
Sodium -wasting disorder(CKD, renal tubular acidosis)

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109
Q

Hyperaldosteronism symptoms

A

Hypertension
Potassium depletion causing fatigue, los of stamina, weakness, conturia, lassitude
THirst and polyuria from hypokalemic nephropathy

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110
Q

Primary hyperaldosteronism conformation test

A

Saline infusion (test for failure of aldosterone suppression)
Plasma aldosterone (put on high Na diet and test urinary aldosterone)
Fludrocortisone challenge to see if aldosterone will suppress

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111
Q

Secondary hyperaldosteronism treatment

A

Salt restriction
Address underlying cause

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112
Q

Adrenal adenoma causing primary hyperaldosteronism treatment

A

Potassium sparing diuretics
HTN control
Management of hypokalemia

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113
Q

Bilateral adrenal hyperplasia causing hyperaldosteronism treatment

A

Bilateral arednalectomy
Aldosterone receptor blockers (spiralactone or eplerenone)
Na channel blockers (Amiloride)

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114
Q

Hypoaldosterone causes

A

Adrenal sestruction
Defects in mineralocorticoid
Inadequate adrenal stimulation
Genetics
Latrogenic
Hyporeninemic hypoaldosteronism

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115
Q

Ion problems in hypoaldosterone

A

Hyponatremia
Hypovolemia
Hypotension
Metabolic acidosis
Hyperkalemia

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116
Q

Where is the thyroid

A

Inferior to cricoid cartilage
Anterior on either side of the neck

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117
Q

Damage to what nerve in thyroidectomy causes vocal cord paralysis

A

Recurrent Laryngeal nerve

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118
Q

TRH

A

Made in hypothalamus
Stimulates ant pit to release TSH

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119
Q

TSH

A

Made in ant pit
Stimulates thyroid to release TH

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120
Q

What thyroid hormone is made most

A

T4

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121
Q

What thyroid hormone is more metabolically active

A

T3

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122
Q

Where are TSH receptors

A

Membranes of follicular cells

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123
Q

Follicular cells of thyroid

A

Make thyroxine (T4) and triiodothyrine (T3)
Cavity between cells filled with colloid called thyroglobulin
Have TSH receptors

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124
Q

Parafollicular cells

A

C-cells between follicles
secrete calcitonin

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125
Q

Reverse T3

A

Not metabolically actie and found more often in stress

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126
Q

T4

A

Thyroxine
Carried in [lasma bound to proteins.
Not as metabolically active
Converted to T3 in peripheral to be used

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127
Q

T3

A

Triiodothyrine
Less protein bound and more active

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128
Q

Normal TSH range

A

0.5-5

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129
Q

What interferes with TSH levels in labs

A

Biotin

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130
Q

Fine needle aspiration

A

Cana be done in office or interventional radiology to get needle biopsy of thymus to check for malignancy

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131
Q

Bethesda classifications for thyroid biopsy

A

I- Repeat FNA
II- clincal follow up
III- Repeat FNA and genetic testing
IV- lobectomy and genetic testing
V- Near total thyroidectomy
VI- Near total thyroidectomy

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132
Q

Thyroscintigraphy

A

Radioactive iodine uptake
Only indicated if pt has HYPERactive thyroid.
Normal is 10-30% at 24 hrs
Oral dose of I123
High uptake with no zones means graves disease
Low uptake means thyroiditis

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133
Q

Cold nodule

A

Nodule on thyroid that has very little iodine uptake.
Could be malignant

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134
Q

Hot nodule

A

Nodule on thyroid that has lots of iodine uptake
Usually benign

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135
Q

Goiter

A

enlargement of thyroid gland
Happens in hypothyroidism to compensate for lack of thyroid hormone.
Happens in hyperthyroidism to make thyroid hormone
Nodular goiters enlarge as function of increased tissue mass as result of nodules

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136
Q

Most common cause of goiter world wide

A

Iodine deficiency

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137
Q

Most common cause of goiter in US

A

Autoimmune

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138
Q

Goiter presentation

A

Lump in neck
Hoarseness
Dysphagia
Neck pain
Dyspnea

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139
Q

Goiter physical exams findings

A

Nonetender enlargement of thyroid gland or nodule
Other symptoms of hypo/hyperthyroid state

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140
Q

What to do if pt comes in with goiter

A

Order TSH, free T4, total T3
Evaluate size and cahracteristics on ultrasound
Radioactive iodine uptake scan if hyperthyroidism
Fine needle aspiration if indicated by TIRADS

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141
Q

How big does nodule have to be for radiofrequency or alcohol ablation

A

> 3cm

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142
Q

Thyrotoxicosis

A

Another word for hyperthyroidism

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143
Q

Primary hyperthyroidism labs

A

Low TSH
High T4 and T3

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144
Q

Secondary hyperthyroidism

A

High TSH
High T4 and T3
Rare
Problem in ant pit

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145
Q

Signs and symptoms of hyperthyroidism

A

Weight loss
Tachycardia
Stare
Lid lag
Sweating
Anxiety
Irritability
Palations
Abd pain
Fatigue

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146
Q

What to do if hyperthyroidism is causing eyes to bulge out

A

MRI of orbits to see extraocular muscles

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147
Q

Methimiazole

A

Antithyroid/thioamide med
Inhibits thyroid synthesis in thyroid gland

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148
Q

Propylthyouracil (PTU)

A

Antithyroid/thioamide
Used in first trimester of pregnancy
Inhibits thyroid hormone synthesis of thyroid gland
Can decrease conversion from T3 to T4

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149
Q

Beta-blockers in antithyroid

A

Controls adrenergic symotomes
Once daily atenolol or metoprolol
High dose of propranolol decreases conversion of T4 to T3

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150
Q

Dexamethasone and hydrocortisone use in antithyroid

A

Decreases peripheral conversion of T4 to T3 and can alleviate pain in thyroiditis

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151
Q

Most concerning side effect of methimazole or PTU

A

Agranulocytosis (not making WBC)

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152
Q

Graves disease pathophys

A

Most common hyperthyroidism
Autoimmune antibodies bind to TSH receptors causing overproduction of T4 and T3
More common in women 20-40
Elderly get apathetic hyperthyroidism and cardiac issues

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153
Q

Graves disease physical exa

A

Warm skin
Fine tremor
Tachycardia
Goiter
Proptosis, stare, lid lag
Thyroid acropachy, onycholysis, pretibial myxedemaI

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154
Q

Thyroid eye disease treatment

A

Refer to ophthalmology
DO NOT treat with radioactive iodine

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155
Q

Graves disease treatment

A

Symptomatic treatment with beta-blockers.
Methimazole or PTU
Radioactive iodine therapy if no opthalmopathy
Total thyroidectomy

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156
Q

Thyroid storm symptoms

A

Agitation
Delirium
High fever
Vomiting
Diarrhea
Dehydration

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157
Q

What can thyroid storm cause

A

Life threatening
Heart failure
Sinus tachycardia
V-fib
MI
Cardiogenic shock

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158
Q

Thyroid storm treatment

A

Beta blocker
PTU

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159
Q

Toxic adenomas and toxic multinodular goiter pathophys

A

Hyperthyroidism
95% benign
Exacerbated by radionuclide study

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160
Q

Toxic adenoma and toxic multinodular goiter findings

A

Nodule(s)
Low TSH
High T3 and maybe T4
Usually no antibodies

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161
Q

Toxic adenoma and toxic multinodular goiter treatment

A

Beta-blockers
Methimazole
Radioactive iodine
Surgical excision

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162
Q

Thyroiditis

A

Inflammation of thyroid causing damage to thyroid follicles and uncontrolled release of thyroid hormone into blood stream

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163
Q

Thyroiditis presentation

A

First presents as hyperthyroidism then resultas in hypothyrooidism or reverts to euthyroid
Low iodine uptake

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164
Q

Thyroiditis treatment

A

NSAIDs
Steroids
Beta-blockers

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165
Q

Four types of thyroiditis

A

Autoimmune
Painful
Infectioussuppurative
IgG4

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166
Q

Types of autoimmune thyroiditis

A

Chronic lymphocytic/Hashimoto’s
Postpartum
Painless (silent) subacute
Meds, iodine, illness

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167
Q

Risk factors for autoimmune thyroiditis

A

Head-neck external beam radiation
Turner syndrome
Hepatitis C
Iodine supplementation
Tobacco use

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168
Q

Post-partum thyroiditis treatmet

A

Symptomatic hyperthyroidism
Short term hormone replacement

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169
Q

Post-partum thyroiditis risk factors

A

High TPO antibodies
T1DM
Other autoimmune

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170
Q

Painful subacute thyroiditis presentation

A

Tender thyroid gland with painful dysphagia.
Same clinical course as post-partum
Usually follows URTI
Could have fever and skin involvement (abscess)
Elevated WBC, ESR,, CRP

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171
Q

Painful subacute thyroiditis treatment

A

NSAIDs or steroids for pain

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172
Q

Thyrotoxicosis facitia

A

Caused by overtreatment or abuse of T4
Low TSH, high T4
RAI uptake abscent

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173
Q

Hydatidiform mole

A

Excess productono f HCG having TSH-like activity
Gestational trophoblastic disease
Low TSH high T4

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174
Q

Struma Ovarii

A

Ovarian teratoma containting thyroid tissue.
Low TSH high T4
RAI uptake in pelvis

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175
Q

Medications associated with hyperthyroidism

A

Iodine supplementation
Amiodarone
Tyrosine kinase inhibitors
Immune checkpoint inhibitors

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176
Q

Types of hypothyroidism

A

Hashimoto
Secondary
Subclinical
Euthyroid sick syndrome
Cretinism
Myxedema

177
Q

Signs and symptoms of hypothyroidism

A

Weight gain
Dry skin
Thinning hair
Thinning nails
Bradycrdia
Skin palor
Puffy face
Goiter
Decreased body temp
Fatigue
Menorrhagia
Constipation
Myalgia and cramps

178
Q

Hypothyroid physical exam findings

A

Periorbital edema
Dry skin
Dry, brittle nails
Edema/lymphedema

179
Q

Levothyroxine

A

BEST
Initial treatment of primary and secondary hypothyroidism
Take on empty stomach
No other food or meds for 30-60 mins
Monitor labs every six weeks until dose stable
Pregnancy increases needs by 30%

180
Q

What is the goal TSH for someone you’re giving levothyroxine

A

1.0 (low, normal range)

181
Q

How to determine dosing for levothyroxine

A

0.75 mcg/lb/day

182
Q

What dose to start elderly person at on levothyroxine

A

50-75 mcg daily

183
Q

Armour Thyroid, Nature-Thyroid, NP Thyroid

A

Mixed T3 and T4 from pigs (porcine)
60-65 mg = 100mcg of levothyroxine

184
Q

Liothyrine

A

Synthetic T3
Metabilized more quickly than T4 so dosed twice daily
25mcg = 100 mcg of levothyroxine

185
Q

Most common hypothyroidism in US

A

Hashimoto
From antibodies against gland

186
Q

Hoshimoto treatment

A

Thyroid hormone replacement

187
Q

Subclinical hypothyroidism

A

Elevated TSH
Normal T4
Can resolve itself
No treatment needed unless TSH is extremely high or if pt is having symptoms

188
Q

Nonthyroidal illness syndrome

A

Low T4 and T3
Normal TSH
High reverse T3
Seen in severe illness
Increased metabolism of T4 and decrease of thyroid binding immunoglobulin
No treatment, recheck labs in 6 weeks

189
Q

Congenital hypothyroidism (cretinism)

A

High TSH
Low T4
Detected in newborn

190
Q

Congenetal hypothyroidism (cretinism) cause

A

THyroid gland agenesis or thyroid hormone receptor resistance

191
Q

Congenital hypothyroidism symptoms

A

Poor feeding
Hypotonia
Enlarged tongue
Cardiac malformation
Possibly permanent cognitive impairement

192
Q

Myxedema cause

A

Long standing untreated hypothyroidism
20-50% mortality

193
Q

Myxedema presentation

A

Hypothermia
Hypotension
Bradycardia
Hypoxia
Lethargy
Psychosis
Coma

194
Q

Myxedema treatment

A

Levothyroxine 200-400mcg
Admission to ICU

195
Q

Myxededma increased susceptibility

A

Bacterial pneumonia
Megacolon
Rhabdomyolysis
Renal impairmnt
Respiratory arrest
Cardiomegaly (myxedema heart)

196
Q

Thyroid cancer presentation

A

Asymptomatic
Hard, fixed, painless mass in neck <5cm
Recent onset with rapid growth
Lymphadenopathy
Hoarsenss
Odynophagia

197
Q

What to do if someone comes in with possible thyroid cancer

A

Check TSH
Ultrasound
FNA if needed

198
Q

Thyroid cancer types in order of common to least common
Also least dangerous to most dangerous

A

Papillary
Follicular
Medullary
Anaplastic

199
Q

Follicular thyroid cancer

A

Associated with autosomal dominant cowden syndrome (loss of tumor suppressor)

200
Q

Medullary thyroid cancer

A

Associated with MEN 2A and 2B
Secrete calcitonin used as tumor marker
Discontinue GLP anlalogs

201
Q

Anaplastic thyroid cancer

A

Least common and most dangerous
Rapidly enlarging mass in multinodular goiter
Metastasizes to adjacent nodes and distant sites

202
Q

Treatment for thyroid cancer

A

Thyroidectomy]
Then radioactive iodine if high risk
T4 replacement keeping TSH slightly low
Deep neck ultracsound every 6-12 months for five years
Monitor TSH ensuring it stays a little low
Test for thyroglobulin adn calcitonin
RAI total body scans

203
Q

Radioactive iodine total body scans

A

Measure thyroglobulin and thyroglobulin AB
Locak or metastatic lesions will take up RAI

204
Q

Thyroidal peroxidase (TPO)

A

Oxidizes iodine so it can be used in TH production

205
Q

Where is T4 converted to T3

A

Liver and Kidney

206
Q

TH MOA

A

T4–>T3
T3 binds to binds to nuclear receptor altering gene expression

207
Q

Entire process of making TH

A

TRH binds to receptor on follicular cell
Increases iodide uptake from Na/I symporter.
Increases synthesis and secretion of thyroglobulin
TPO converts Iodide into iodine
TPO links iodine with tyrosine residues on thyroglobulni to make MIT and DIT
TPO connects DIT with another DIT or MIT
Proteolytic enzymes cleave T3 and T4 from thyroglobulin

208
Q

Osmolarity

A

Osmoles per liter of solvent

209
Q

Osmolality

A

Osmoles per kg of solvent

210
Q

Tonicity

A

Describes osmolality of solution

211
Q

SIADH

A

Post pit releases too much ADH (AVP)

212
Q

Diabetes insipidus

A

Post pit releases not enough ADH (AVP) or kidneys not responding to ADH (AVP)

213
Q

ADH (vasopressin) physiology

A

Acts on V2 receptors in principal cells of collecting ducts to stimulate aquaporin expression
Aquaporin 2 moves water down osmotic gradient from collecting duct into principal cell
Aquaporin 3 and 4 move water out of principal cell into medullary extracellular fluid and circulation

214
Q

What causes release of ADH

A

Increased plasma osmolality
Decreased intravascular pressure

215
Q

Renal response to ADH

A

Increase concentrated urine
Decrease diluted urine

216
Q

ADH effect on vasculature

A

Vasoconstriction to increase BP

217
Q

What regulates thirst

A

Osmostat in anteromedial hypothalamus

218
Q

Causes of SIADH

A

Small cell lung carcinoma
Uterine carcinoma
Thymoma
Drugs
INfection
Pulm disorders

219
Q

SIADH pathophys

A

Water retention
natriuresis (Na loss)

220
Q

SIADH lab presentation

A

Hyponatremia
Hypotonic
High urine osmolality
High urine Na
High specific gravity
Normal blood volume

221
Q

SIADH symptoms

A

Nausea, malaise, muscle cramps
Headache, lethargy, weakness
Cerebral edema, confusion, AMS, seizure, resp distress

222
Q

SIADH testing

A

Water load then assess urine osmolality

223
Q

SIADH treatment

A

Fluid restriction
Hypertonic saline
V2 receptor agonist
Demeclocycline
Fludrocortisone

224
Q

Primary polydeipsia cause

A

Patient drinking a lot of water

225
Q

Central diabetes insipidus cause

A

Decreased ADH secretion
Hypothalamus lesion
Post pit tumor
Lung or breast tumor
Head trauma
Infectious diseas

226
Q

Nephrogenic diabetes insipidus cause

A

Decreased renal response to ADH
Renal disease
Sickle cell
Renal ischemia
Nephrotoxic drugs

227
Q

Central diabetes insipidus pathophys

A

Hypofunction of hypothalamus or post pit
Urinary free water excretion (polyuria)
Increased plasma osmolality
Hypernatremia

228
Q

Nephrogenic diabetes insipidus

A

Decreased renal responsivness to ADH
Urinary free water excretion (polyuria)
INcreased plasma osmolality
Hypernatremia

229
Q

Diabetes insipidus lab presentation

A

Hypernatremia
Polyuria
Low urine osmolality

230
Q

Diabetes insipidus clinical findings

A

Lots of dilute urine
Excessive thirst (polydipsia)

231
Q

Diabetes insipidus diagnostic test

A

Water deprivation test
Desmopressin stimulation test

232
Q

Water deprivation test

A

Test for diabetes insipidus
Decrease water intake and check urine volume and concentration.
Positive test if urine remains diluted and low urine osmolality and lots of volume.

233
Q

Desmopressin stimulation test

A

Shows what type of diabetes insipidus
Give desmopressin
Measure urine volume 12 hrs before and 12 hrs after.
Central diabetes insipidus will have decreased urine output
Nephrogenic diabetes insipidus will have no response

234
Q

Neuroendocrine cell

A

Epithelial cell that recieces messages from nerons and releases hormones

235
Q

Neuroendocrine tumors (NET)

A

Slow growth (indolent)
Mostly nonfunctional
Rare (37 per mil)

236
Q

What does over 90% of GEP-NET’s have that help us with treatment

A

High concentrations of somatostatin receptors.
We can image with octreotide or other radionucleotides

237
Q

Most common NET

A

1.Gastrointestinal treact (GiNET)
2. Pancreatic (PNET)
3. Lung

238
Q

NET cause

A

Familial
25% associated with MEN1
MEN 1-4
Von Hippel-Landau Syndrome
Neurofibromatosis (NF 1)

239
Q

NET clinical presentation

A

Depends on location
many asymptomatic
Carcinoid syndrome

240
Q

Carcinoid syndrome

A

Classic NET
Small bowel (midgut) most common)
Increased serotonin, histamine, prostaglandin

241
Q

Carcinoid syndrome symptoms

A

Abd pain
DIarrhea
Skin flushing (after meals)
Bronchospasm if in lung

242
Q

GiNET

A

Gastrointesitinal NET
Type I - most common with chronic atrophic gastritis and pernicious anemia
Type II - 5% gastrinomas and MEN1
Type III - 20% more aggressive
Type VI - Chronic PPI use and less malignant

243
Q

Small intestinal GiNET

A

Usually ileum
Abd pain
often misdiagnosed IBS

244
Q

Appendix GiNET

A

Usually neoplasm of appendix
Almost always found accidentally in appendectomy

245
Q

Colorectal GiNET

A

Most discovered by accident in colonoscopy

246
Q

PNET (pancreas)

A

20% alpha (glucagon)
70% beta (insulin)
5% D cells (gastrin or somatostatin)
5% F cells (pancreatic polypeptide)

247
Q

NET diagnosis

A

Stepwise
Labs show it
CT scan
Biopsy
PET with Ga-68 DOTA-peptide for staging and restaging

248
Q

NET treatment

A

Surgery if not metastatic
Somatostatin analog therapy
Lutathera
Chemo (only for high grade (fast growing))

249
Q

Carcinoid syndrome treatment

A

Surgery id possible
Somatostatin analog therapy

250
Q

Pheochromocytoma

A

Rare catecholamine-secreting tumor in adrenal medulla

251
Q

Pheochromocytoma symptoms

A

Extreme uncontrollable HTN
All sympathetic nervous symptom stuff bc release catecholamines (epi and norepi)

252
Q

Pheochromocytoma cause

A

Multiple Endocrine Neoplasy type 2 (MEN2)
Von hippel-lindau syndrome
Neofibromatosis type I

253
Q

Classic triad of symptoms for pheochromocytoma

A

Episodic headache, sweating, tachycardia

254
Q

Best test for pheochromocytoma diagnosis

A

24 hr fractionated catecholamines and metanephrines
Plasma fractionated metanephrines (more sensitive)
CT or MRI (>10 HU on noncontrast)

255
Q

Surgical treatment for pheochromocytoma

A

Laparascopic adrenalectomy

256
Q

Pheochromocytoma pre-op treatment

A

Combined alpha (phenoxybenzamine) and beta adrenergic blockade 7 days before surgery(START WITH ALPHA FIRST)
Beta just couple days before

257
Q

Phenoxybenzamine

A

Alpha blocker used in pheochromcytoma pre-op
Nonselective

258
Q

Metyrosine

A

Decreases catecholamine production in pheochromocytoma pre-op
Blocks tyrosine hydroxylase preventing conversion of tyrosine to dopamine

259
Q

Adrenal incidentaloma

A

Mass greater than 1cm found accidentally on adrenal gland when looking for something els.
Look to see if it is malignant or functional (secretes something)

260
Q

Tumors of adrenal cortex

A

Adrenocortical adenoma
Adrenocortical carcinoma

261
Q

Tumors of adrenal medulla

A

Neuroblastoma
Pheochromocytoma

262
Q

Characteristics of benign adenoma

A

Less than 4 cm
ROund and smooth
Homogenous
Located in cortex
Unilateral less concerning

263
Q

At what size adrenal mass do you refer to surgery

A

> 10cm

264
Q

MEN1 associated tumors

A

Parathyroid hyperplasia
Pituitary adenomas
Pancreatic NET
Other NET

265
Q

What issue happens in 90% of MEN1 patients

A

Hyperparathyroidism

266
Q

Pituitary adenoma

A

Secrete prolactin in 60% of MEN1 tumors

267
Q

MEN2 cancers

A

Medullary thyroid cancer
Pheochromocytoma

268
Q

Common symptoms of Type 1 diabetes mellitus

A

polydipsia
polyuria
Hunger
Dry skin
Drowsy
Blurry vision
Slow healing

269
Q

Common signs of Type 1 Diabetes mellitus

A

Diabetic ketoacidosis
Hyperglycema
Hyperkalemaia
Hyponatremia
Glucosuria
Ketonuria
Metabolic acidosis

270
Q

Diagnostic tests of T1DM

A

Fasting plasma glucose >126
Random plasma glucose >200
Hemoglobin A1C >6.5
3 hour glucose tolerance test >200
C-peptide
Autoimmune markers
Ketonemia/ketonuria

271
Q

Stage 1 T1DM

A

Autoimmunity
normoglycemia
Antibodies present
No treatment

272
Q

Stage 2 T1DM

A

Autoimmunity
Dysglycemia
Presymptomatic
Antibodies present
Teplizumab for treatment

273
Q

Stage 3 T1DM

A

New-onset hyperglycemia
Symptomatic
Standard treatment

274
Q

Honeymoon phase of T1DM

A

Soon after starting insulin therapy
Temporary recovery of beta cell function for about a year.
Educate patient to continue testing blood glucose because it will eventually end

275
Q

Musculo skeletal problems with T1DM

A

Charcot’s joint
Cheiroarthropathy
Adhesive capsulitis
Carpal tunnel
Dupuytren contractures
Amputation

276
Q

Neonatal diabetes

A

Occurs by 6 months of ae.
Life long condition but don’t always need insulin
Small fetuses for gestational age

277
Q

Cystic fibrosis related diabetes

A

Result of pancreatic scarring
20% of CF pts
Treated with insulin

278
Q

Ketosis-prone type 2 diabetes

A

Autoantibody negative
Inherited
Episodic DKA with varying degrees of insulin deficiency between episodes

279
Q

Postpancreatitis diabetes

A

From pancreatic scaring
Treated with insulin

280
Q

What does A1C measure

A

glycemic control over 2-3 months
Remember it is an average so doesn’t tell the whole story

281
Q

Goal A1C for adult with T1DM

A

7%

282
Q

Goal A1C for child

A

6.5% if can be done without lows
7% normal
8% if history of sever lows

283
Q

Goal A1C for elderly

A

7-7.5%
8-8.5% if difficult

284
Q

What does fructosamine level measure

A

Glucose control over 1-2 weeks when A1C is unreliable

285
Q

Continuous glucose monitor

A

Measures interstitial glucose levels constantly
(Dexcom)

286
Q

What all is prescribed in finger stick glucose monitoring

A

Meter
Test strips
Lancet

287
Q

Time in range

A

Percent of day when bllood sugar is between 70-180
High TIR correlates with lower A1C
Low TIR correlates with microvascular complications

288
Q

Time in range goal

A

70%

289
Q

T1DM treatment

A

INSULIN
pramlintide
GLP-1 agonists
SGLT-2 antagonist
Teplizumab

290
Q

Where to inject insulin

A

Fatty tisssue
Upper posterior arm
Abdomen
Buttocks
Thigh
Best to spread around where you give a shot bc of lipohypertrophy

291
Q

Insulin pumps

A

Use basal insulin drip throughout day.
Can change rate of insulin

292
Q

Basal bolus regimen

A

Multiple daily injections of insulin to mimic body’s basal bolus activity
Basal is dose taken in morning and it kind of stays with you.
Bolus is jump in insulin at meals

293
Q

How much bolus insulin should be given based on carbs

A

1 unit per 10 grams of carbs each meal

294
Q

When should bolus shot be given

A

Less than 15 minutes before meal

295
Q

How much does one unit of insulin drop blood glucose

A

30 points

296
Q

Dawn phenomenon

A

Morning hyperglycemia from natural cortisol and GH rise

297
Q

Somogyi effect

A

Nocturnal hypoglycemia results in surge on counterrregulatory hormones causing hyperglycemia

298
Q

Metabolic causes of hypoglycemia

A

INsulinoma
Hypothyroidism
Addison’s disease
Liver failure
Alcoholism
Malnutrition
Renal failure
Beta cell proliferation
Alpha cell fatigue
IGF-2 and GLP-1 secreting tumors

299
Q

Diabetic meds that can cause hypoglycemia

A

Insulin
Sulfonurea
Glinides
SGLT2 inhibitors
GLP-1 analogs

300
Q

Meds that can cause hypoglycemia

A

Floroquinolones
Beta blockers
Ace inhibitors

301
Q

When does seizure happen from hypoglycemia

A

Sugar less than 30

302
Q

Common symptoms of hypoglycemia

A

Shaky
Sweaty
Dizzy
COnfusion
Hungry
Weakness
Headache
Nervous

303
Q

Fasting hypoglycemia

A

5 or more hours after eating
Related to basal insulin
Sulfonylurea use
Insulinoma

304
Q

Post-prandial hypoglycemia

A

Reactive
Within 2 hours after meal
Related to bolus insulin
Common in rapid weight loss surgery

305
Q

Behaviooral hypoglycemia

A

Stacking of insulin doses
Delivered bolus too early before getting meal
Alcohol induced
Activity induced

306
Q

How to treat hypoglycemia orally

A

Eat/drink 15g of carbs
Wait 15 mins
Check blood
Repeat if still low

307
Q

How to treat severe hypoglycemia

A

IM or intranasal glucagon
IV D50 (50% dextrose)

308
Q

Insulinoma

A

Over 99% in Isle of Langerhans
90% are benign
From MEN1

309
Q

Signs and symptoms of insulinoma

A

Fasting hypoglycemia
Anxiety

310
Q

Insulinoma treatment

A

Surgery

311
Q

Insulinoma diagnosis

A

Elevated C peptide levels
CT and MRI

312
Q

Euglycemic DKA

A

DKA with normal blood sugar
Associated with SGLT-2 inhibitors

313
Q

DKA

A

Diabetic ketoacidosis
Body can’t utilize glucose so ketoacids are accumulated because of lipolysis (gluconeogenesis)

314
Q

What patients have DKA

A

Usually T1DM but can be seen in T2DM
Also can be caused by infection, trauma, MI, surgery, bad insulin, not taking insulin

315
Q

Symptoms of DKA

A

Polyuria
Polydipsia
Hypotension
Fruity breath

316
Q

Lab finidngs in DKA

A

Hyperglycemia
Hperkalemia
Hyponatremia
Elevated BUN
Elevated creatinine
Hyperphosphatemia

317
Q

Normal serum osmaolality

A

280-300

318
Q

DKA treatment

A

Restore plasma volume with normal saline until BG gets to 250 switch to D5
Give potassium even though its high
Give insulin

319
Q

HHNS

A

Hyperglycemic Hyperosmolar Nonketotic Syndrome
Normal aniongap

320
Q

What patients normally getn HHNS

A

Type 2 diabetics

321
Q

HHNS cause

A

Partial or relative insulin deficiency causes hepativ glucose output.
Massive fluid loss related to osmotic diuresis results in renal impairment

322
Q

Lab findings of HHNS

A

Hyperglycemis
Hyponatremia
Hyperkalemia
Elevated BUN
Elevated creatinine
Elevated serum osmolality

323
Q

HHNS signs and symptoms

A

Weakness
Polyuria
Polydipsia
Dehydration
Nausia
Coma
Confusion
Convulsion

324
Q

HHNKS treatment

A

Restore plasma volume with half norma saline
Reduce blood glucose without bolus
Fix electrolytes with potassium

325
Q

T2DM

A

Excess lipids in adipocytes lead to insulin resistance
Production of adiponectin (insulin-sensitizing peptide) is reduced and cause increase in glucose production in liver causing fasting hyperglycemia.

326
Q

Post prandial glucose

A

After meal glucose
Utilized by skeletal muscle
Insulin stimulates glucose uptake

327
Q

Cause of T2DM

A

Peripheral insulin resistance
Increased hepatic glucose production
Impairment of insulin secretion

328
Q

What can cause falsely low A1C

A

IV iron
EPO therapy in CKD
Vitamin C and E

329
Q

What can cause falsely elevated A1C

A

Splenectomy
Hereditary spherocytosis
IDA

330
Q

What A1C is considered prediabetic

A

5.7-6.4%

331
Q

Criteria for screening for T2DM

A

BMI 25+
Fam history
CVD history
HDL cholesterol
HTN
PCOS
Pre-diabetic

332
Q

T2DM signs

A

Fatigue
Blurred vision
Nausea
Polyphagia
Polydipsia
Polyuria
Weight change
Numbness in legs
Metabolic syndrome
40% asymptomatic

333
Q

T2DM physical findings

A

Obesity
HTN
Eye issues
acanthosis nigrans, candida infections
Neuro issues
Dry skin
Muscle atrophy
Claw toes
Ulcer

334
Q

T2DM chronic macrovascular complications

A

Coronary artery disease
Carotid artery/cerebrovascular disease
Peripheral artery disease

335
Q

T2DM chronic microvascular complications

A

Neuropathy
Nephropathy

336
Q

What’s the risk of T2DM patient to have MI

A

Same as someone without T2DM who has had an MI
They have elevated plasminogen activator inhibitors and fibrinogen that can cause thrombosis

337
Q

T2DM peripheral vascular risk

A

Ischemia of lower extremities
Erectile disfunction
Intestinal angina

338
Q

Neuropathy

A

in 50% of pts with T2DM
Myelinated and unmyelinated fibers lost
Usually bilateral
CN 3,4,6 involvementA

339
Q

Autonomic neuropathy

A

Long standing DM
Orthostatic hypotension
Gastroparesis
Incontinence
ED
Hypoglycemia unawareness

340
Q

Neuropathy clinical testing

A

Pin prick for small fiber function
Vibratory sense for large fiber function
Monofilament test for protective sensation

341
Q

Charcot foot

A

Structural changes to foot from neuropathy

342
Q

Neuropathy management

A

Alpha lipoic acid
B12 replacement
Tricyclic antide[ressants
Calcium channel modulators
Serotonin norepinephrine reuptake inhibitors

343
Q

Diabetic nephropathy

A

T2DM
Microalbuminuria
Pts have high risk of diabetic retinopathy
Macroalbuminuria over next 10 years in 50% of pts

344
Q

Nephropathy diagnostic test

A

Spot urine for microalbumin/creatinine ratio
Creatinine every three months
Refer to nephrology if macroalbuminuria >300mg/day or eGFR<30

345
Q

Leading cause of blindness between ages of 20-74

A

Diabetes mellitus

346
Q

VEGF in diabetes

A

Causes production of new blood vessels in retina associated with retinopathy of DM

347
Q

Proliferative retinopathy presentation

A

Cotton wool spots from growth of new capillaries and fibrous tissue in retina and vitreous cahmber
More common T1DM

348
Q

Nonproliferative retinopathy presentation

A

Earliest stage
Microaneurysms, dot hemorrhages, exudates, retinal edema

349
Q

How to treat chronic complications of T2DM

A

Glucose control
Treat HTN with ACEi/ARBs, diuretics
Treat cholesterol with statins
Weight management

350
Q

What predicts mortality of T2DM

A

A1c levels within three months of initial diagnosis
So follow up more often than three months until pt gets stable

351
Q

What is the first drug for patients with T2DM and obesity

A

Metformin

352
Q

Metformin

A

1 drug for T2DM and obesity

Decreases insulin resistance
Decreases hepatic gluconeogenesis
Don’t give pt with GFR<30
Can cause Vitamin B12 deficiency and hypoglycemia
Weight neutral

353
Q

DPP4 inhibitor

A

T2DM
-gliptin
increases and prolongs incretin hromone activity
INcrease insulin release and reduce glucagon secretion
Post-prandial glucose
Weight nutral

354
Q

GLP-1 agonsit T2DM

A

-glutide
Post prandial glucose
Weight loss
Lowers A1C by 1.5

355
Q

Rybelsus

A

Semaglutide as weekly oral agent

356
Q

SGLT2 inhibitors

A

-flozin
Lowers renal glucose threshold causing more glucose excretion in urine
Weight loss
Lowers A1C by 1%
Not for pts with GFR>30
Reduction in microaluminuria
Used in HF pts

357
Q

Sulfonylureas

A

Glipizide and glimepiride most common
Glyburide not for people over 65
Increase insulin secreetion and decrease hepatic glucose production
Post prandial glucose
Weight gain
Lowers 1C by 1%

358
Q

Thiazoolidinediones

A

Pioglitazone
Reduces circulating fatty acid concentration.
Lower glucose by increasing muscle, fat, and liver’s sensitivity to insulin.
Not for people with heart problems
Fasting and post prandial glucose
Weight gain
Lowers A1c by 1%

359
Q

Exubera adn Afrezza

A

Inhaled insulin
Quick acting

360
Q

Soliqua

A

Combo of fixed doses of basal insulin and GLP-1
Lixisenatide is the GLP-1 inside

361
Q

What meds to give pt with ASCVD for T2DM

A

GLP-1 (-glutide)
SGLT-2 (-gliflozin)

362
Q

What med to give pt with heart failure for T2DM

A

SGLT-2 (-gliflozin)

363
Q

What med to give pt with CKD for T2DM

A

SGLT-2 (-gliflozin)

364
Q

Gestational diabetes cause

A

Insulin secretory capacity not sufficient to overcome insuln resistance created by anti-insulin hormones secreted by placenta during pregnancy

365
Q

Safest way to treat and monitor pregnant pt with hyperglycemia

A

Insulin

366
Q

Babies born to mothers with uncontrolled blood sugar

A

Usually premature and weigh >9lbs
Baby at risk of hypoglycemia and jaundice
Should be screened every 1-3 years for diabetes

367
Q

Maturity-onset diabetes of the young (MODY) symptoms

A

Polyuria
Polydipsia
Dehydration
Blurry vision
Recurrent skin/yeast infection
Nonobese

368
Q

Diabetic med control pre-op

A

Pre-op visit if A1c < 8%
Metformin held day of surgery
SGLT-2 held 3-4 days before surgery
GLP-1 held one week before surgery

369
Q

Preferred insuln treatment for non-critically ill pateints

A

basal plus bolus

370
Q

Fequently usd medications that can elevate glucose levels

A

Corticosteroids
Beta-blockers
Thiazide diuretics
Antipsychotics
Statins

371
Q

IGF-1 release sequence

A

GHRH from hypothalamus
GH from ant pit
IGF-1 from liver

372
Q

IGF-1 function

A

Increase muscle size, bone size, and endochondral ossification.
INcreases activity of collagen, proteoglycans, osteoblasts, and osteoclasts

373
Q

Gigantism

A

Excess GH before puberty

374
Q

Acromegaly

A

Excess GH after puberty

375
Q

Acromegaly cause

A

Ant pit adenoma

376
Q

Acromegaly clinical manifestations

A

Little effect on stature and height
Growth of bones
Suddenly shoes, gloves, hats, rings don’t fit
Soft tissue swelling
Organ enlargement
Thyroid goiter/megaly
Hyperhydrosis “moist handshake”
Hirsutism
Visual probs
Small dick from co-secretion of prolactin
Decreased libido

377
Q

Gigantism clinical manifestations

A

Abnormal growth

378
Q

Acromegaly/Gigantism lab diagnostics

A

Increased IGF-1
Glucose suppression test to see if rise in GH
MRI of pituitary
Prolactin
GLucose, A1C
CMP
TSH, T4

379
Q

Acromegaly complications

A

Carpal tunnel
DM
CHF
HTN
Colon polyps
Difficult intubation
Sleep apnea from pharynx/larynx enlargement

380
Q

Acromegaly/gigantism management

A

SURGICAL EXCISINO
CABERGOLINE if not
Octeotride and lanreotide
Pegvisomant

381
Q

Growth hormone deficiency cause

A

Pituitary tumor or treatment from pituitary tumor
Extrapituitary tumor
Sarcoidosis
Sheehan syndrome

382
Q

What adults should be evaluated for GH deficiency

A

Known hypothalamic or pituitary disease
History of pediatric GH deficiency

383
Q

Congenital GH deficiency clinical manifestations

A

Short stature (2 SD below mean)
Slow development
Hypoglycemia, jaundice, and hypogonadism in new borns

384
Q

Pediatric GH deficiency clinical manifestations

A

Slow growth
Distinct facial features
Central obesity
Delayed puberty
Webbed neck
Short limbs compared to trunk

385
Q

Adulthood GH deficiency clinical manifestations

A

Central obesity
Depression
Mem probs
Decreased lean body mass
Decrease bone and mineral density
Increased risk for cardiovascular disease

386
Q

Pediatric growth hormone deficiency diagnostics

A

Growth assessment (charts)
A projected height that differs more than 10 cm from parents suggest possible problem

387
Q

GH deficiency lab studies

A

Low IGF-1
GH provaction testing where GH should be made to rise by meds

388
Q

GH deficiency management

A

Early diagnosis
Recombinant human GH ASAP (Norditropin once daily or lonapegsomatotropin, somopacitan, or somotrogon once weekly)
Can be stopped whenever goals are met
Assess growth every 3-6 months and bone age every 1-2 yrs

389
Q

Male primary hypergonadism

A

Disease of testes
Low testosterone and/or sperm count
High LH and/or FSH

390
Q

Secondary hypogonadism

A

Disease of pituitary or hypothalamus
Low testosterone and/or sperm count
Normal or low LH and/or FSH

391
Q

Male Hypogonadism symptoms in adolescents

A

Appear younger
Small genetalia
Difficult in gaining muscle mass
Lack of facial hair
High pitch voice

392
Q

Male hypogonadism in adults

A

Decreased energy and libido
Decreased muscle mass and body hair
Hot flashes
Gynecomastia (most likely primary)
Infertility
Testes decrease in size in primary

393
Q

Male hypogonadism diagnosis

A

Unequivocally low serum total testosterone concentrations between 8 and 10am on at least two occasions
<300

394
Q

Most important single test to evaluate for testosterone

A

Serum testosterone

395
Q

Male hypogonadism free testosterone

A

18-69 y/o: <35
70+ y/o: <30

396
Q

Testosterone replacement contraindications

A

No low testosterone
ActiveActive breast or prostate cancer
Untreated sleep apnea or heart failure

397
Q

Klinefelter syndrome

A

47, XXY (47 chromosomes with extra X)
Most common cause of primary hypogonadism
Destruction of seminiferous tubules and leydig cells causing decreased sperm and testosterone production

398
Q

Klinefelter syndrome symptoms

A

Long legs and arms
Sparse body hair
Small testes
Infertility
Gynecomastia
Not present until after puberty

399
Q

Klinefelter syndrome therapy

A

NOT for prepubertal boys.
Start at age 13 until growth ceases or until 18-19 to cause genetal development, facial and pubic hair, muscle development, and growth
Full doses of testosterone replacement for adult men

400
Q

Gynecomastia

A

Males develop breast tissue
Pseudo is just fat tissue

401
Q

Signs of malignancy in gynecomastia

A

Asymetry
Nipple retraction
Bleeding
Discharge

402
Q

Gynecomastia labs

A

Liver tests
BUN
Creatinine
Endocrine testing
Serum prolactin
Estradiol
hCG

403
Q

Gynecomastia imaging

A

Mammography or chest CT

404
Q

Gynecomastia treatment

A

Reassure and observe during puberty
Remove drug causing it
Raloxefine or anaastrazole if persistent
Surgery last resort

405
Q

Primary amenorrhea

A

Absence of menarche by age 15
Or absence of menarche and no breast tissue at 13

406
Q

Secondary amenorrhea

A

3 consecutive months without menses in women who previously had regular menses or 6 months in women with irregular menses

407
Q

Primary amenorrhea cause

A

Gonadal dysgenesis (turner syndrome)
Vaginal agenesis

408
Q

Turner syndrome

A

Most common sex chromosome abnormality in females
Loss of part of X chromosome (45,X-)
Early ovarian failure

409
Q

Turner syndrome symptoms

A

Short stature
Broad chest
Short and webbed neck
Kyphoscoliosis

410
Q

Secondary amenorrhea cause

A

Pregnancy
PCOS

411
Q

Primary amenorrhea treatment

A

Treat underlying cause
Help achieve fertility if desired
Estrogen replacement

412
Q

Primary amenorrhea diagnostics

A

hCG, FSH, TSH, PRL
MRI of pituitary
Pelvic US
Karyotype to check for turners

413
Q

Secondary amenorrhea labs

A

hCG, FSH, TSH, PRL
Estradiol
Testosterone

414
Q

Secondary amenorrhea treatment

A

Treat underlying cause
Help achieve fertility if desired
Estrogen replacement
(same as primary)

415
Q

Hirsutism

A

Male pattern hair growth on women

416
Q

Hirsutism cause

A

PCOS

417
Q

Virilization

A

Development of male physical characteristics in women

418
Q

Hirsutism and virilization treatment

A

Oral contraceptives (combined estrogen-progestin)
Spironolactone
Laser hair removal

419
Q

Ovarian germ cell tumor presentation

A

Abd enlargement
Abd pain
Precocious puberty from hCG production
Fever
Vaginal bleeding

420
Q

Ovarian germ cell tumors

A

Pelvis US
Tumor markers (hCG and AFP elevated)

421
Q

Prader-Willi syndrome

A

Hypopituitarism
Paternal chromosome 15 deleted or unexpressed

422
Q

Prader-Willi syndrome

A

Trouble sucking or swallowing
Floppy bable
Abnormal facial features
Mental development delay
Short stature
Hyperphagia or morbid obesity
Hypogonadism

423
Q

Kallman syndrome

A

Hypopituitarism
Defective hypothalamic gonadotropin-releasing hormone causes low LH and FSH

424
Q

Kallman syndrome clinical presentation

A

Delayed or absent puberty
Color blindness
Ansomnia
Optic atrophy
Cleft palate
Renal probs
Cryptorchidism
Neurologic abnormalities like mirror movements

425
Q

Sheehan’s syndrome

A

Hypopituitarism
Postpartum pituitary gland necrosis
No lactation
Decreased PRL

426
Q

What ACTH value shows pituitary failure

A

<10

427
Q

Test for pituitary failure

A

Insulin tolerance testing

428
Q

Most common cause of hyperpituitarism

A

Pituitary adenoma

429
Q

Pituitary adenoma

A

Most common cause of hyperpituitarism
slow growing
Can put pressure on optic chiasm causing periferal vision loss
Functioning means it secretes hormone
Micro is <1cm macro is >1cm
Macro more common

430
Q

Pituitary adenoma symptoms

A

Headache
Vision probs
NV
Changes in behavior
Nasal

431
Q

Pituitary adenoma diagnosis

A

Check hormones
MRI or CT

432
Q

Pituitary adenoma treatment

A

Transphenoidal pituitary microsurgery EXCEPT PROLACTINOMAS
Radiation if persistent or can’t have surgery

433
Q

Hyperprolactinemia cuase

A

PRL secreting tumor
Pregnancy
Meds
Familial

434
Q

What is most common pituitary tumor

A

Prolactinoma

435
Q

Main pharamacologic cause of hyperprolactinemia

A

Antipsychotics
Antidepressants
Anti HTN

436
Q

Hyperprolactinemia symptoms

A

Fatigue, depressoin
Hypogonadism, decreased libido, impotenc, nnfertility, gnecomastia in men
Galactorrhea, infertility, oligomenorrhea, amenorrhea in women

437
Q

Prolactinoma treatment

A

Dopamine agonist (Cabergoline)

438
Q
A

PAS 531 (10 decks)

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