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GI/Endo/Repro > Assessment 4 > Flashcards

Assessment 4 Flashcards

1
Q

Classic endocrine glands

A

Pituitary
Adrenal
Thyroid
PTH glands

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2
Q

Atypical endocrine glands

A

GI
Adipose
Kidney, heart, liver,

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3
Q

Classes of hormones

A

Peptide/protein

Steroid

Amine

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4
Q

Steroid hormone precursor

A

Cholesterol

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5
Q

Amine hormone precursor

A

Tyrosine or Tryptophan

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6
Q

Hormone receptor types

A

Ion channel linked

Enzyme linked

Nuclear receptor

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7
Q

Regulation of hormone production

A

Biosynthesis regulation

Precursor processing

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8
Q

Regulation of hormone secretion

A

Feedback loops

Cyclical variation

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9
Q

Protein binding

A

Extends half life of hormone
Protect from degradation
Solubilize lipophilic compounds

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10
Q

Hormone clearance

A

Hepatic clearance/metabolism

Renal filtration

receptor mediated endocytosis

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11
Q

Target tissue hormone regulation

A

Receptor population

Upregulation vs downregulation of receptors

Only tissues with specific receptors will respond

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12
Q

Pituitary gland anatomical location

A

Inferior to hypothalamus

Enclosed in sella turcica

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13
Q

Parts of Pituitary gland

A

Anterior: Adenohypophysis
Posterior: Neurohypophysis

Connected to hypothalamus via pituitary stalk

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14
Q

Median eminence

A

Inferior border of hypothalamus

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15
Q

Posterior PG embryology

A

Arise from diencephalon

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16
Q

Anterior PG embryology

A

Arise from oral ectoderm

Envagination = rathke’s pouch

Normally loses connection to oral ectoderm

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17
Q

Rathke’s cysts

A

Usually benign

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18
Q

Craniopharyngioma

A

Benign and rare

Headache, vision issues, hormone deficiency

Surgery or radiation

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19
Q

Anterior PG blood supply

A

Parvocellular neurons from hypothalamus, end at median eminence

Hormones secreted into portal vessels which act on anterior PG

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20
Q

Posterior PG blood supply

A

Magnocellular neurons extend from hypothalamus into PPG

Synthesize and secrete ADH and Oxytocin and store in PPG

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21
Q

Hypothalamic pituitary GH axes

A

Hypothalamus (GHRH) –> APG (GH) –> Liver (IGF-1)

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22
Q

Hypothalamic pituitary Thyroid axes

A

Hypothalamus (TRH) –> APG (TSH) –> Thyroid (T3, T4)

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23
Q

Hypothalamic pituitary adrenal axes

A

Hypothalamus (CRH) –> APG (ACTH) –> Adrenal (Cortisol)

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24
Q

Hypothalamic pituitary gonadal axes

A

Hypothalamus (GnRH) –> APG (LH/FSH)

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25
Q

Prolactin

A

Promotes alveolargenesis during pregnancy

Post partum: Milk synthesis/secretion

Estrogen = (+)
Dopamine = (-)
Negative feedback on itself

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26
Q

Prolactinoma

A

Most common pituitary adenoma

Pharmacological intervention: Dopamine agonists

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27
Q

Sheehan syndrome

A

Complication of post partum hemorrhage

APG enlarged but blood supply same during pregnancy –> infarction from hypovolemic shock due to hemorrhage

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28
Q

Sheehan syndrom presentation

A

Acute: fail to lactate, hypotension, tachycardia

Chronic/Late: Amenorrhea, hypothyroidism

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29
Q

ADH

A

Vasopressin

Increase water permeability in kidneys: V2 receptor, aquaporin channel

Vascular smooth muscle contraction: V1 receptor

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30
Q

Oxytocin

A

Milk ejection
Uterine contraction

Stimulated by suckling, infant, orgasm

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31
Q

Action of growth hormone - Liver

A

Increase RNA, protein, glucose, IGF synthesis

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32
Q

Action of growth hormone -adipose

A

Lipolysis

Decrease glucose uptake

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33
Q

Action of growth hormone - muscle

A

Increase AA uptake and protein synthesis

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34
Q

IGF action

A

Increase organ size/function
Linear growth
Increase lean body mass

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35
Q

Categories of GH secretory factors

A
  1. Hormones
  2. Neural
  3. Metabolic
  4. Pharm
  5. Other
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36
Q

GH and metabolism

A

Fasting/starving or decreased glucose concentration = more GH

Increase glucose = low GH

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37
Q

Gonadotroph

A

Clinically non function pituitary adenoma, gonads

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38
Q

Thyrotrophs

A

Central hyperthyroidism or clinically non functioning

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39
Q

Lactotrophs

A

Hyperprolactinemia

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40
Q

Somatotrophs

A

Acromegaly

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41
Q

Corticotrophs

A

Cushings

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42
Q

Hyperprolactinemia clinical mainifestations

A

Decrease LH/FSH via GnRH inhibition

Infertility/galatctorrhea/amenorrhea

Impotence, decreased libido (men)

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43
Q

Gigantism vs acromegaly

A

GH excess

Acromegaly = epiphyseal closure
Gigantism = no closure
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44
Q

Acromegaly diagnosis

A

IGF-1

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45
Q

Acromegaly treatment

A

Somatostatin analog (GH inhibitor)

GH receptor antagonist

Radiotherapy

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46
Q

Cushings syndrome vs disease

A

Syndrome: Symptoms caused by prolonged exposure to glucocorticoids

Disease: Pituitary corticotroph adenoma

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47
Q

Cushings disease

A

Hypersecretory Corticotroph adenoma causing excess adrenal secretion

Fat face/body

Excess ACTH

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48
Q

Cushings diagnosis

A

24hr urinary free cortisol
Late night salivary cortisol
Dexamethasone suppression test

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49
Q

Thyrotropin secreteing pituitary adenoma

A

Lab: High free T4 and T3, abnormally high TSH

Weight loss, diarrhea, tremors, palpitations/tachycardia

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50
Q

TSH deficiency signs/symptoms

A

Decrease in energy
Growth retardation
Constipation
Weight gain

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51
Q

Hypopituitarism treatment

A

Relief of mass effect

Replacement of hormones

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52
Q

Central diabetes insipidus

A

Excessive free water loss due to lack of ADH

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53
Q

21 alpha hydroxylase deficiency

A

Most common CAH (90-95% of cases)

  1. Decreased cortisol
  2. Increased androgens in utero (virilization of female fetus)
  3. Decreased aldosterone –> salt wasting. Decreased Na and increased K
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54
Q

11 beta hydroxylase deficiency

A

2nd most common CAH

  1. Decreased cortisol
  2. Increased mineralocorticoid activity (high 11-DOC)
  3. Increased androgens in utero

Either 1+2 or 1+2+3

Diagnose with increased 11 DOC in urine

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55
Q

Lipoid CAH

A

Rare CAH

Defect in P450scc or StAR

Buildup of cholesterol

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56
Q

Vasopressin hypofunction

A

Diabetes insipidus: cannot excrete concentrated urine

Neoplasm
Inflammation
Head trauma

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57
Q

Vasopressin hyperfunction

A

SIADH: Cannot excrete dilute urine –> hyponatremia and volume expansion

Ectopic secretion from tumors

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58
Q

Conn syndrome

A

Primary aldosteronism with hypertension and unprovoked hypokalemia

Suppression of renin

Most commonly due to aldo secreting adenoma

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59
Q

CAH

A

Congenital adrenal hyperplasia

Cortisol deficiency and ACTH increase

90% cases associated with 21 hydroxylase deficiency

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60
Q

Adrenal cortical carcinoma

A

Rare neoplasm

Necrosis and hemorrhage

Invasion of adjacent structures: IVC, adrenal vein

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61
Q

Adrenal gland hormones: medulla

A

Catecholamines

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62
Q

Adrenal gland hormones: cortex

A

Mineralocorticoids
Glucocorticoids
Androgens

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63
Q

Zona glomerulosa hormones

A

Mineralocorticoids

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64
Q

Zona fasciculata hormones

A

Glucocorticoids

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65
Q

Zona reticularis hormones

A

Androgens

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66
Q

Aldosterone function

A

Salt/water retention

K excretion

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67
Q

Primary aldosteronism

A

Aldosterone production is abnormally high

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68
Q

Primary aldosteronism physiological symptoms

A

HTN
Hypokalemia and mild hypernatremia
Mild metabolic alkalosis

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69
Q

Primary aldosteronism causes

A

Aldo producing adrenal adenoma (APA)

Adrenal hyperplasia (IHA, BAH, UAH)

Familial hyperaldosteronism

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70
Q

Screening test for primary aldosteronism

A

PAC/PRA > 20 = (+)

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71
Q

Primary aldosteronism confirmation tests

A

Oral sodium loading
IV NS load
Fludicortisone suppression

Check to see if aldo is suppressed

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72
Q

Primary aldosteronism subtype classification tests

A

CT: Can test cause (adenoma, hyperplasia, carcinoma) but not source

Adrenal vein sampling: Compare aldo from both sides, can find source

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73
Q

Right vs left adrenal vein

A

Right: Short and small. Directly enters IVC

Left: Tributary to real vein, easy to cannulate

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74
Q

Adrenal vein sampling results

A

Aldosterone concentration/Cortisol concentration

4:1 = unilateral

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75
Q

APA/IHA treatment

A

Surgery in good candidates

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76
Q

IHA/GRA treatment

A

Minrealocorticoid receptor blocker - Spironolactone

Secondary antihypertensive

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77
Q

Pheochromocytoma and Paraganlioma

A

Paraganglioma arise from autonomic ganglia, outside of adrenal glads

Excess production of epi and norepi

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78
Q

Pheochromocytoma and Paraganlioma incidence

A

90% adrenal
90% unilateral
90% benign
15-20% familial

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79
Q

Paraganglioma stats

A

Norepi excess

30% malignant
25% extra abdominal

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80
Q

Presentation of Pheochromocytoma

A 
Pain
Pressure (HTN)
Perspiration
Pallor
Palpitations
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81
Q

Pheochromocytoma diagnosis

A

Metanephrine plasma level

24hr urinary metanephrine, fractioned catecholamines

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82
Q

Pheochromocytoma radiology

A

CT scan

MIBG: Compound that resembles Norepi, scan can detect tumors

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83
Q

Adrenal failure clinical presentation

A

Hyperpigmentation: Skin, buccal cavity, scars

Postural hypotension

Addisonian crisis

Nausea/vomiting

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84
Q

Hyperpigmentation w/ primary adrenal insufficiency?

A

Melanocyte stimulating hormone and ACTH on part of same protein

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85
Q

Adrenal failure lab findings

A

Hyperkalemia, hyponatremia, hypoglycemia

Lymphocytosis, eosinophilia

Adrenal autoantibodies if auto immune disease

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86
Q

Primary adrenal failure

A

Addisons

Decreased aldo and decreased cortisol, issue with adrenal gland

Hyperkalemia, hypotension

Increase ACTH

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87
Q

Secondary/tertiary adrenal insufficiency

A

Normal aldo, less prominent hypotension

Decreased ACTH, no hyperpigmentation

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88
Q

Primary adrenal insufficiency etiology

A 
Autoimmune
Infection
Cancer
Adrenal hemorrhage
CAH
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89
Q

Secondary adrenal insufficiency etiology

A

Glucocorticoid withdrawal

Hypopituitarism via radiation, surgery, mass

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90
Q

Low cortisol + Low ACTH =

A

Secondary adrenal insufficiency

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91
Q

Low cortisol + High ACTH =

A

Primary adrenal insufficiency

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92
Q

Most common CAH enzyme deficiencies

A

21 hydroxylase
11B hydrolxylase
17a hydroxylase

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93
Q

21 a hydroxyalse deficiency symptoms

A

Virilizing + Salt wasting

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94
Q

Cortisol and metabolism

A

Gluconeogenesis and glucose storage, decrease glucose breakdown

Lipolysis but also increase appetite

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95
Q

ACTH independent vs dependent Cushings

A

Dependent: Cushings disease
Ectopic ACTH
Ectopic CRH

ACTH independent: Adrenal adenoma/carcinoma/hyperplasia
Exogenous steroids

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96
Q

Thyroid blood supply

A

Superior thyriod artery
Inferior thyroid artery
Lowest thyroid artery
- Branch of brachiocephalic trunk, present in 5-10%

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97
Q

Recurrent Laryngeal nerves

A

Innervate muscles of larynx, open/close vocal cords

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98
Q

T3 and T4 action

A

T3 is better ligand for receptor

T4 is negative feedback on hypothalamus

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99
Q

T3/4 synthesis

A
  1. Iodide uptake via NIS
    2a. Thyroglobulin synthesis and exocytosis into follicle - not driven by TSH

2b. Free iodide transported into follicle by Pendrin
- Iodide oxidized by TPO to iodine

  1. Iodination of thyroglobulin = MIT and DIT
    - TPO
  2. TSH stimulated conjugation of iodinated tyrosines to make T3 and T4
  3. Endocytosis of iodinated thyroglobulins, lysoendosome formed
  4. Proteolysis in lysoendosome releases T3, T4, RT3. MIT/DIT recycled
  5. Secretion into circulation
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100
Q

DIT + DIT =

A

T4

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101
Q

MIT + DIT =

A

T3, most active

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102
Q

DIT + MIT =

A

reverse T3

Useless sack of shit

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103
Q

Thyroid transport proteins

A

Thyroxine binding globulin (TBG) - T3, T4

Trasnthyretin - Thyroxine

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104
Q

Calcium sensing receptor

A

Highly expressed on chief cells of parathyroid gland

Sense serum Ca concentration

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105
Q

Vit D

A

Diet or synthesized via cholesterol

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106
Q

Vit D and Ca

A

Vit D increases Ca transport proteins in duodenum

107
Q

PTH synthesis

A

Prohormone, processed in golgi

PTH increases serum calcium

108
Q

PTH and bone

A

Induces RANK ligand and M-CSF on osteoblasts

Activate osteoclast precursor cells which become osteoclasts –> eat up bone and release Ca

109
Q

PTH and kidney

A

Ca reabsorption in DCT and CCD

110
Q

PTH related protein

A

PTHrP

Binds PTH receptor, mobilize Ca to produce milk

Mediates osteolytic bone metastasis

111
Q

Calcitonin

A

Less bone resorption and decreased Ca released

112
Q

Mutations in CaSR

A

Inactive: Hypercalcemia/hypocalciuria

Active: Hypocalcemia

113
Q

Leptin

A

Produced in fat

Circulating levels signal to brain how much fat is in system

114
Q

Melanocortin system

A

alpha-MSH (agonist) and AgRP (antagonist)

AgRP = increased feeding/body weight

a-MSH = reduced feeding and body weight

115
Q

Diet and melanocortins

A

Diet = aMSH down and AgRP up

116
Q

Leptin deficiency and melanocortins

A

MSH down

AgRP up

117
Q

High fat leptin pathway

A

Leptin activates POMC –> MC4 receptor –> decreased weight

Inhibits AgRP

118
Q

Low fat leptin pathway

A

Low leptin does not stimulate POMC, less AgRP inhibition –> Activate Y1/Y5 –> Increase weight

AgRP also inhibits MC4 receptor

119
Q

Leptin and thyroid function

A

Leptin is positive regulator of TRH

Increase Leptin = increase Thyroid

120
Q

Leptin and gonads

A

Positive regulator

Increase leptin = increase LH/FSH

121
Q

Environmental causes of obesity

A

Genetics modified by environment

Obesogenic environment: Inactivity and readily available food supply (increased portions, energy dense)

122
Q

Obesity guidelines: Waist circumference

A

Measure in pts with BMI of 25-34.9

> 35in (female)
40in (males)

Estimate of visceral fat

123
Q

Obesity guidelines: Assess and treat CV risk factors and comorbidities

Weight loss vs maintenance

A

Weight loss: Overweight + 1 or more CV factor OR obese

Weight maintenance: Normal weight, overweight w/o comorb, overweight/obese but cant lose weight

124
Q

Obesity guidelines: Recommend goals for weight loss

A

Initial goal: 10% weight loss in 6 months

Rate of weight loss:

.5-1 lb/week BMI (27-34.9)

1-2 lb/week (BMI>35)

125
Q

Obesity guidelines: Recommend method for weight loss

A

Weight loss with both low carb and low fat diets

Diets should be tailored to individual patients

126
Q

Obesity guidelines: Comprehensive lifestyle interventions

A

1200-1500kcal/day for females

1500-1800 kcal/day for men

500-700kcal/day energy deficit + increased activity

127
Q

Acceptable macronutrient Distribution range

A

Carb: 45-65%
Protein: 10-35%
Fat: 20-35%

128
Q

Thyroid hypofunction histology

A

Atrophic follicles

Mononuclear cell infiltration with germinal centers

129
Q

Subacute thyroiditis

A

Granulomatous (painful)

Lymphocytic (painless)

130
Q

Riedels thyroiditis

A

Rare, fibrotic

131
Q

Acquired thyroid hypofunction

A

Post therapy for hyperthyroidism or thyroid neoplasms

132
Q

Thyroid hyperfunction

A

Thyrotoxicosis

Increased production or increased release of pre formed hormone from damaged thyroid gland

133
Q

Hyperthyroidism (increased production)

A

Autoantibody that mimics TSH (Graves)

Excess TSH or TRH (very rare)

Secretion by neoplasm

134
Q

Thyroid storm

A

Life threatening

Fever, delirium, seizures, vomiting

Death from cardiac arrhythmia/failure

Treat by block T4–> T3 conversion

135
Q

Nodular hyperplasia

A

Usually euthyroid

Dominant nodule may emerge, simulate neoplasm

Iodine deficiency
Dietary goitrogens

136
Q

Thyroid anaplastic carcinoma

A

Aggressive tumor in elderly

Kills by direct invasion of airway

May have p53 loss

137
Q

RAS point mutation cancer

A

Fillicular and anaplastic carcinoma

138
Q

PTEN point mutation

A

Follicular and anaplastic carcinoma

139
Q

BRAF point mutation

A

Papillary carcinoma

140
Q

RET gene mutation

A

Papillary carcinoma

Medullary carcinoma

141
Q

Hypoparathyroidism most common cause

A

Surgical excision of parathyroid gland

142
Q

Hypoparathyroid causes

A

Surgery
Congenital agenesis/hypoplasia
Autoimmune
Mg deficiency

143
Q

Hypoparathyroid biochemical features

A

Low PTH
Low Ca
High phosphorus

144
Q

Hypoparathyroid clinical features

A

Increased neuromuscular excitability
Emotional disorders
Parkinson like syndrome
Basal ganglia calcification

145
Q

Hyperparathyroidism causes

A

Adenoma (80%)
Hyperplasia (15%)
3% of all cases associated with MEN I or IIa

146
Q

Secondary hyperparathyroidism causes

A

Chronic renal insufficiency
Vit D deficiency
Intestinal malabsorption

147
Q

Secondary hyperparathyroidism and renal failure

A

Renal retention of phosphorus + loss of Ca

Reduced 1,25(OH) Vit D resulting in decreased Ca absorption

148
Q

Advanced hyperparathyroidism

A

Severe kidney stones

Osteitis fibrosa

149
Q

Malignancy associated hypercalcemia

A

80% due to direct invasion of bone by tumors

20% attributed to PTHrP: Blocks osteoprotegrin secretion by osteoblasts –> Promotes osteoclastogenesis

150
Q

pH and Calcium serum concentration

A

Alkalosis = increase in albumin bound Ca but decrease in free Ca

Acidosis = Decrease in albumin bound Ca but increase in free Ca

Lower pH = Decreased albumin affinity for Ca

151
Q

Hypercalcemia clinical presentation

A

Kidney Stones

Bones - osteitis fibrosa, fractures

Moans - lethargy, depression

Ab Groans - constipation, peptic ulcer

152
Q

Osteitis fibrosa

A

Increased osteoclasts

increased bone resorption

153
Q

Hypercalcemia diagnosis

A

Check serum Ca

Check PTH level

Measure 24hr urinary Ca after repleting Vit D to rule out FHH

154
Q

HyperPTH treatment

A

PTH surgery

Bisphosphonates: Anti resorptive agents (bone protection)

Cinacalcet: Decrease serum Ca level (symptomatic hypercalcemia)

155
Q

Hypocalcemia pathogenesis

A

Deficiency Vt D supply/action

Deficient PTH synthesis/secretion

156
Q

Normal Vit D level and required amount

A

> 30ng/mL

Need ~2000IU

157
Q

Imparied PTH secretion causes

A

Antibody inhibition
CaSR activating mutation
Hyper/hypomagnesemia
PTH gene mutations

158
Q

DiGeorge Syndrome clinical pres

A 
Cardiac
Abnormal fascies
Thymic aplasia
Cleft palate
Hypocalcemia with 22q11 deletion
159
Q

Hypocalcemia and neuromuscular

A

Lower threshold to nerve conduction = spasms, cramps, weakness

160
Q

Chvosteks sign

A

Hypocalcemia

Press on cheek = twitch of face

Response = degree of hypocalcemia

161
Q

Trousseau’s sign

A

Place BP cuff on upper arm –> carpopedal spasm

162
Q

Treatment of hypocalcemia

A

Raise serum Ca to low-normal range

Avoid hypercalciuria

IV Ca, oral Calcitrol

Vit D, maybe Mg

163
Q

Lobectomy/hemi thyroidectomy

A

Removal of one lobe

Diagnostic for suspicious nodules

Toxic adenoma

164
Q

Total/near total thyroidectomy

A

Removal of entire thyroid - leave small remnant near nerve/PT

Cancer, graves

165
Q

Thyroid surgery complications

A

Recurrent laryngeal nerve injury: Unilateral = hoarse, bilateral = airway obstruction

Superior laryngeal nerve injury: Loss of high pitch

Hypocalcemia/hypoPTH

Hemorrhage - cut open to prevent airway obstruction

166
Q

Neck/Node dissection: Central

A

Level VI

Initial lymph drainage of thyroid

Elective or therapeutic: Positive or negative nodes

167
Q

Neck/Node dissection: Lateral

A

Levels I-V

Secondary lymph drainage of thyroid - Jugular, transverse cervical

Therapeutic - positive for nodes

168
Q

PTH surgery

A

Unilateral: sporadic primary hyperPTH

Bilateral: Both sides, non localized primary hyperPTH, hereditary (MEN1, MEN2a)

Secondary/tertiary hyperPTH

169
Q

Indications for PT surgery

A

Bones
Stones
Muscle weakness

170
Q

Parathyroid embryology: Inferior

A

3rd pharyngeal pouch
Descend with thymus
Anterior to recurrent laryngeal nerve

171
Q

Parathyroid embryology: Superior

A

4th pharyngeal pouch

Posterior to recurrent laryngeal nerve

172
Q

Primary HyperPTH MEN

A

MEN1: hyperplasia
MEN2a: multiple adenomas

173
Q

Minimally invasive/unilateral parathyroidectomy benefits

A

Reduced risk

Positive preop localization

High cure rates

174
Q

Intraoperative PTH assay

A

Helps in deciding when to stop procedure

Pre incision and pre removal level with post removal

80% reduction = specific

50% reduction = sensitive

175
Q

Pancreatic islet cell types

A

Beta cells - Insulin

Alpha cells - Glucagon

Delta cells

176
Q

Proinsulin –> insulin

A

Proinsulin cleaved to insulin (A+B) and C peptide

177
Q

Incretin effect

A

GLP-1 and GIP - gut hormones

Dietary glucose –> GLP-1/GIP activation –> insulin secretion/glucagon inhibition

178
Q

Insulin action

A

Insulin binds to receptor –> MAP kinase pathway –> Glucose transporter to membrane

179
Q

Low glucose effect

A

Low glucose –> Decreased ATP/ADP –> KATP channel open –> weak Hyperpol –> Ca channel open –> Ca increase glucagon secretion

180
Q

High glucose effect

A

High glucose –> ATP/ADP increase –> KATP channel close –> depol –> no glucagon release

181
Q

Type I diabetes overview

A

Morbidity and mortality

Autoimmune destruction of islets

Absence of insulin

Genetic+environment

No cure

182
Q

Type I Diabetes autoimmunity

A

Selective destruction of islet Beta cells

Circulating antibodies to islet cell antigens

Linkage with MHC genes

T cell mediated beta cell destruction

183
Q

T cell mediated Type I DM

A

Infiltrating CD4+, CD8+ T cells

anti T cell therapies are effective

184
Q

Genetic factors of T1D

A

MHC Class II locus

Defects in immunomodulation

Attack own cells

185
Q

DCCT results

A

Control of blood glucose works with intensive treatment - But difficult therapy

186
Q

Hypoglycemia

A

Rate limiting factor for T1D treatment

Severe hypoglycemia sees unawareness of symptoms

187
Q

Causes of hypoglycemia

A

Absolute excess insulin: Before lunch/dinner, predawn, gastroparesis

Relative excess: Exercise and alcohol

188
Q

Exercise and glucose

A

Increase exercise = glucose into tissues = hypoglycemia risk

189
Q

T1D routine management

A 
HA1c multiple times a year
Foot exams/neuropathy testing
Renal monitoring
Retinal exams
Lipids
BP
190
Q

LADA

A

Latent autoimmune diabetes of adulthood

In between DM1 and DM2

Variable auto immune function, metabolic syndrome, insulin resistance

191
Q

Diabetic ketoacidosis

A

Hyperglycemia
Acidosis
Volume depletion
Electrolyte abnormalities

192
Q

Diabetic ketoacidosis management

A

Volume replacement
Insulin
Electrolyte balance
Education

193
Q

Diabetic ketoacidosis pathogenesis

A

Decrease in insulin: Increase glucose, decreased glucose uptake –> hyperglycemia = osmotic diuresis

Increased FFA release, increased ketogenesis = ketoacidosis

194
Q

DKA symptoms and signs

A

Symptoms: Polyuria, weakness, weight loss, nausea, vomiting

Signs: Tachycardia, hypothermia, ileus, acetone breath, altered sensorium, Kussmaul (deep, frequent) breaths

195
Q

Prognostic factors of DKA

A

Hypotension
Age over 65
Altered mental status

196
Q

DKA management

A 
Hydration
IV insulin
Monitor K
Bicarb for extreme cases
Prevent recurrence: Education
197
Q

Primary hypothyroidism etiology

A

Autoimmune
Thyroidectomy
Iodide deficiency
Drugs

198
Q

Secondary hypothyroidism etiology

A

Hypopituitarism

Hypothalamic damage

199
Q

Clinical manifestations of hypothyroidism

A 
Weakness 
Lethargy
Slow speech
Cold intolerance
Constipation
Weight gain
Hair loss
Edema
Decreased perspiration - dry skin
200
Q

FT4 normal

TSH normal

201
Q

FT4 low

TSH High

A

Primary hypothyroidism

202
Q

FT4 low

TSH normal/low

A

Secondary hypothyroidism

203
Q

Subclinical hypothyroidism

A

T4 normal
Slightly high TSH
Few or no symptoms

204
Q

Hypothyroidism therapy

A

Treat with hormone replacement

LT4 pills = synthetic T4

Check TSH 6-10 weeks

Target is TSH level

205
Q

Thyroxine dosage

A

Higher weight = higher dose

Old patients on lower dose

Ca, Fe, soy can block absorption

Malabsorption = higher doses

Estrogen, antidep, anti seizure = increase requirement

206
Q

Hypothyroidism in pregnancy

A

Thyroxine is safe

Dosage increases during pregnancy

Baby cant make thyroid hormone during first trimester

Important to keep regulated during pregnancy

207
Q

Thyroid autoimmunity

A

Most common cause of hypothyroidism

Graves disease

Anti TPO antibodies (Hashimoto)

TRAB and TSI (Graves)

208
Q

Thyrotoxicosis etiology

A

Graves

Toxic Adenoma

Subacute/silent thyroiditis

TSH secreting adenoma

Factitious/Iatrogenic (taking thyroid hormone)

209
Q

Graves disease

A

Autoimmune hyperthyroidism

Female predominance

Associated opthalmopathy

210
Q

Clinical manifestations of Graves

A 
Nervous
Fatigue
Weakness
Heat intolerance
Tremor
Hyperactivity
Palpitations
Increase appetite
Weight loss
211
Q

Lid lag

A

Hyperadrenergic effect of thyrotoxicosis

212
Q

Graves opthalmopathy

A

Eyes bulge forward, eyelid retraction

Autoimmune response against orbital auto antigen shared by thyroid

213
Q

Toxic multinodular goiter

A

2nd most common cause of hyperthyroidism, most common in elderly

Dysphagia, hoarseness, shortness of breath

214
Q

Thyroiditis: Subacute and Silent

A

Acutre destruction of thyroid tissue, leakage of hormone

Subacute: painful, viral illness

Silent: post partum, painless, pre existing autoimmune

215
Q

TSH secreting pituitary adenoma

A

Rare
Macroadenoma
Elevated T4
Inappropriately normal TSH

216
Q

Factitious thyrotoxicosis

A

Due to ingestion of thyroid hormone

Serum thyrogolubulin used for diagnosis

Exogenous thyrotoxicosis: low thyroglobulin

Destructive thyroiditis: high thyroglobulin

217
Q

Increased radio iodine uptake = ?

A

Graves

Toxic MNG

Toxic adenoma

218
Q

Decreased radio iodine uptake = ?

A

Thyroiditis

Exogenous thyroid hormone

Iodinated contrast

219
Q

Thionamides

A

Treatment for hyperthyroidism

Methimazole and PTU block thyroid hormone formation - Block TPO

PTU decreases T4–>T3 conversion

220
Q

Radioiodine treatment

A

Preferred treatment
NOT in pregnancy
Eventual hypothyroid

221
Q

Sick Euthyroid Syndrome

A

Decrease in T3/T4/TSH but increase in rT3

Decreased 5 deiodinase

Decreased TBG

Plasma inhibitors to binding

Increased TBG

Decrease uptake of thyroid hormones

222
Q

Pheochromocytoma treatment

A

Adrenalectomy - high risk, need to prepare

223
Q

Cushings disease clinical presentation

A

Thin skin, acne, bruising, hirtuism

Hypertension

Depression

Moonface, buffalo hump, truncal obesity, thin limbs

Hyperglycemia, osteoporosis, hypokalemia

224
Q

Cushings treatment

A

Transsphenoidal surgery – Pituitary irradiation –> Total bilateral adrenalectomy

225
Q

Adrenal tumor disease treatment

A

Surgical resection –> Mitotane therapy –> Surgery of recurrent tumor –> Enzyme inhibitors

226
Q

Ectopic ACTH syndrome treatment

A

Surgical resection –> Adrenal enzyme inhibitor –> Medical/surgical adrenalectomy

227
Q

Epidemiological determinants of T2DM

A

Genetic risk factors

Demographics

Behavioral/lifestyle

MEtabolic determinants

Intermediate risk categories: insulin resistance, glu inteolerance

228
Q

Diagnostic testing for diabetes

A

Fasting blood glucose: Normal 200

Random plasma glucose: >200

HbA1C: Normal 6.5%

229
Q

HbA1C

A

Measure of glucose binding to Hb in blood

Accurate representation of 3 months glu level

230
Q

T2DM organ pathophysiology: Liver, Muscle, Adipose, Pancreatic islet

A

Liver: Increased hepatic Glu production

Muscle: Decreased Glu uptake

Adipose: High lipolysis even with increased insulin

Islet: Glucagon high after meal, insulin doesn’t increase as much

231
Q

Ominous octet

A
  1. Increased hepatic production of glucose
  2. Decreased incretin effect
  3. Increased lipolysis
  4. Increased kidney Glu reabsorption
  5. Decreased Glu uptake by muscle
  6. Neurotransmitter dysfunction
  7. Increased glucagon secretion
  8. Impaired insulin secretion
232
Q

Natural history of Type 2 diabetes and Beta cell function

A

Insulin resistance increases

Genetic Beta cell dysfunction increases over time and eventually reaches failure

233
Q

Mechanisms of insulin resistance

A 
Elevated FFA
Increase muscle TG
Abnormal mitochondrial function
Hyperinsulinemia
Inflammation and TNFa
Hyperglycemia
Lipodystrophy
234
Q

Lack of insulin and lipids

A

Adipose metabolism without insulin inhibition = elevated TG, reduced HDL, small dense LDL particles

Atherogenic

235
Q

Treatment of diabetes goals

A

HbA1C target less than 7%
Diet/lifestyle modification
Medication
Manage CV risks

236
Q

Diet recommendations for T2DM

A

Caloric restriction for obesity

Limit CHO to 45-60g

Limited saturated fat

Increase dietary fiber

237
Q

Gestational diabetes

A

Glucose intolerance during pregnancy

7-10% pregnancy

Progressive insulin resistance

Failure of beta cell compensation

238
Q

Gestational DM diagnosis

A

Screening: Glucose challenge

100g OGTT if over threshold of glucose challenge

239
Q

SGLT2 Inhibitor

A

Blocks reabsorption of glucose in kidney

Dapaglifozin

240
Q

Thiazolidinidiones

A

Activate PPAR-gamma

Decrease FFA, increase insulin sensitivity

CHF issues
Weight gain

241
Q

Secretagogues

A

SUR-1 activator: Block KATP channel –> insulin release

Sulfonylureas - Glipizide. Cheaper/lower dose

Meglitinide - Nateglinide

Weight gain, hypoglycemia

242
Q

Biguanides

A

Metformin

Activate AMPK = increase glucose uptake by muscle/decrease hepatic gluconeogenesis

Lactic acidosis, GI issues

243
Q

DPP4 inhibitor

A

Slow degradation of GLP-1/GIP

Sitagliptin, Linagliptin

Well tolerated, high cost

244
Q

Alpha glucosidase inhibitor

A

Block CHO digestion (final step)

Acarbose

Diarrhea/flatulence

245
Q

GLP-1 agonist

A

Increase GLP-1

Dulaglutide

Weight loss, GI, Injection

High cost

246
Q

Amylin mimetics

A

Activate amylin receptor: Decrease glucagon, decrease gastric emptying, increase satiety

Weight loss

Decrease post prandial glucose

High cost

Pramlintide

247
Q

Bile acid sequestrants

A

Bind bile acid

Decrease hepatic glucose production

High cost

Colesevelam

248
Q

Dopamine-2 agonists

A

Modulate hypothalamic control of metabolism

Increase insulin sensitivity

High cost

Bromocriptine

249
Q

Hyperglycemic damage to tissue (4)

A
  1. Increased accumulation of AGE’s
  2. PKC activation
  3. Aldose Reductase pathway acceleration
  4. Hexosamine pathway increase
250
Q

Accumulation of AGE

A

Advanced glycosylated end products

Can diffuse out of cell and damage ECM and alter albumin

Results in pro inflammatory cytokines and growth factor

251
Q

PKC activation

A

Induces PKC pathway

Increase blood vessel constriction

Blood vessel leakiness/angiogenesis

Clot formation and slowing of anti coagulation

Proinflammatory gene expression

252
Q

Aldose Reductase acceleration

A

High glucose is converted to sorbitol by aldose reductase

Enzyme can’t be used to generate glutathione

Low glutathione = increased oxidative stress

253
Q

Hexosamine pathway

A

Glu –> Fru –> F6P –> N acetyl glucosamine

N acetyl glucosamine can alter gene expression and result in pathology of damaging blood vessels

254
Q

Unifying mechanism for hyperglycemia and tissue damage

A

Glucose –> ROS –> PARP –> Decrease GAPDH –> 4 pathways of tissue damage

255
Q

Macrovascular damage mechanism

A

Increased FFA –> ROS –> PARP –> etc etc

256
Q

Diabetic microangiopathy

A

Diffuse thickening of Basement Membrane

Distortion, abnormal permeability, eventual occlusion of capillaries

257
Q

Diabetic retinopathy (2 types)

A

Background (Non proliferative) Retinopathy

Proliferative Retinopathy

258
Q

Non proliferative Diabetic retinopathy

A

Mild – Moderate – Severe

Microaneurysms, hemorrhages, exudates

Macular edema

259
Q

Proliferative Diabetic retinopathy

A

Neovascularization

Pre retinal hemorrhages
Fibrovascular tissue proliferation
Macular edema

260
Q

Diabetic Nephropathy

A

Damage to vessels in renal system

Glomerulosclerosis, thickening of BM, nodular glomerulosclerosis

Nephrotic

261
Q

5 Stages of Diabetic Nephropathy

A
  1. Hyperfunction/hypertrophy
  2. Silent stage - BM thickened
  3. Incipient stage - microalbuminuria
  4. Overt Diabetic nephropathy - macroalbuminuria
  5. Uremic - ESRD
262
Q

Diabetic peripheral neuropathy

A

Nerve damage/destruction

Pain and sensory loss

263
Q

5 Major factors of Diabetic foot

A
  1. Neuropathy
  2. Peripheral artery disease
  3. Ulceration
  4. Infection
  5. Impaired wound healing

GI/Endo/Repro (8 decks)

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