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Endo & Repro block > General > Flashcards

General Flashcards

1
Q

What are the major subtypes of pituitary adenomas?

A
  • Prolactin-producing
  • GH producing
  • ACTH-producing
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2
Q

What is the most common hormone-producing adenoma?

A

Prolactin-producing

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3
Q

T or F: Diabetes insipidus is common in patients with pituitary adenomas.

A

False, check for other sellar lesions

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4
Q

What do lactotrophs make?

A

Prolactin

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5
Q

What do somatotrophs make?

A

GH

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6
Q

What do corticotrophs make?

A

ACTH

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7
Q

What do thyrotrophs make?

A

TSH

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8
Q

What do gonadotrophs make?

A

FSH/LH

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9
Q

What is the most common presentation of a lactotroph adenoma?

A

Amenorrhea/galactorrhea in younger women, mass effects in older

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10
Q

Most common presentation of a corticotroph cell adenoma

A

Cushing’s

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11
Q

Most common presentation of a thyrothroph cell adenoma

A

Hyperthyroidism

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12
Q

Most common manisfestations of a gonadotroph adenoma

A

Mass effect

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13
Q

Most null cell adenomas are probably

A

FSH/LH-producing tumors

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14
Q

What hormones does the posterior pituitary produce? What nuclei does it use?

A

ADH and oxytoxin from the supraoptic and paraventricular nuclei.

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15
Q

What is the normal microscopic appearance of the posterior pituitary?

A

nuclei (pituicites) in a pink (axon) background

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16
Q

Adenomas less than ___ are called microadenomas

A

10 mm

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17
Q

Adenomas more than ___ are called macroadenomas

A

4 cm

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18
Q

Histology of pituitary adenomas

A

Columnar to cuboidal to polygonal, monomorphic round-to-oval nuclei, salt & pepper chromatin

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19
Q

What gene is implicated in pituitary adenomas?

A

MEN-1

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20
Q

Epidemiology of prolactinomas

A

W, 21-40

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21
Q

Prolactinoma symptoms in men

A

Sexual impotence, decreased libido

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22
Q

Prolactinoma symptoms in children

A

Mass effect, growth failure

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23
Q

Prolactinoma symptoms in adolescents

A

Mass effects, pubertal delay, growth arrest (boys), glactorrhea (girls)

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24
Q

Stalk effect will increase serum prolatin up to

A

100 ng/mL

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25
Q

A level of prolactin over ___ indicates and adenoma

A

250 ng/mL

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26
Q

Gross imaging prolactinoma

A

Soft, red-tan

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27
Q

Prolactinoma histology

A

Monomorphic cells, sheet-like architecture, granulated (sparse common or dense), psammoma bodies/amyloid in sparsely granulated

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28
Q

T or F: most prolactinomas are caused by MEN-1

A

False, most are sporadic. Familial cases are usually caused by MEN-1

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29
Q

These adenomas account for 25% of operated tumors.

A

GH adenoma

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30
Q

Cilinal symptoms due to GH adenomas are mediated by

A

GH and IGF-1

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31
Q

Tumor that causes sleep apnea

A

GH adenoma (because of enlargement of tongue and uvula)

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32
Q

Tumor that cuases sleep apnea, LVH, arthalgias, and diabetes

A

GH adenoma

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33
Q

How is a GH adenoma diagnosed?

A

Elevated IGF-1 in the plasma

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34
Q

Gross appearance of GH adenomas

A

Soft, white to grey-red

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35
Q

GH adenoma histology

A

Columnar or cuboidal cells, granules containing GH, keratin filaments (fibrous bodies) if sparsely granulated

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36
Q

Pit adenoma associated with Carney’s complex and MEN-1

A

GH adenoma

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37
Q

T or F: Most GH adenomas are sporadic

A

True

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38
Q

What do ACTHomas make?

A

Proopiomelanocortin (POMC), which is cleaved to form ACTH

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39
Q

Epidemiology of ATCHomas

A

W, 30-40

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40
Q

Abdominal & neck fat, purple striae, insulin resistance, immunocompromised, neuropsyc?

A

Cushing’s

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41
Q

How to diagnose Cushing’s

A

24 hr cortisol urine, demonstrate loss of circadian cortisol secretion

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42
Q

Gross ATCH adenoma

A

Small (usually too small for surgeon to find), red

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43
Q

Histology ATCH tumors

A

Columnar/polygonal cells, small monomorphic nuclei, abundant cytoplasm

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44
Q

What gene is implicated in ATCH adenomas?

A

MEN-1, but most occur sporadically

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45
Q

What is a null cell adenoma?

A

Anterior pituitary tumor with no immunohistochemical demonstration of hormone production

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46
Q

Epidemiology of null cell adenomas

A

Older patients (>40)

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47
Q

How do null cell adenomas present

A

Mass effect, maybe stalk effect, usually very large & cytic on imaging

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48
Q

Gross null cell adenomas

A

Soft, yellow-tan

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49
Q

Null cell adenoma histology

A

Columnar to polygonal, round-oval nuclei, sheet-like

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50
Q

What is pituitary apoplexy?

A

Enlargement of adenoma due to hemmorhage, often with accompanying infarct

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51
Q

What are some signs of apoplexy?

A

Subarachnoid hemorrhage, increased intracranial pressure, headache, visual symptoms (sudden blindness), worsened hypopituitarism

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52
Q

What is a pituicytoma?

A

Neoplasm of pituicites (glial cells of posterior pituitary)

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53
Q

Epidemiology pituicytomas

A

Rare, adults 40-60

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54
Q

Signs of pituicytoma

A

Mass effects

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55
Q

Gross pituicytoma

A

Tan, rubbery, well-curcumscribed

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56
Q

Histology pituiccytoma

A

Elongated bipolar glial cells with elliptical nuclei, intersecting fascicles

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57
Q

How to treat pituicytoma

A

Surgery

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58
Q

How to treat GH adenoma

A

Surgery or somatostatin analogs

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59
Q

What are craniopharyngeomas composed of?

A

Squamous epithelial cells of the sellar region, probably associated with cells in Rathke’s pouch

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60
Q

What are the 2 variants of craniopharyngiomas?

A

Adamantinomatous

Papillary

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61
Q

Which craniopharyngioma variant occurs in children 5-15 and adults 45-60?

A

Adamantinomatous

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62
Q

Which craniopharyngioma occurs in adults 40-55 years old?

A

Papillary

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63
Q

Where are most craniopharyngiomas located?

A

Suprasellar

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64
Q

What are some signs of cranipharyngiomas?

A

Endocrine disturbances (esp in children), diabetes insipidus, elevated intracranial pressure (if 3rd ventricle involved)

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65
Q

Gross cranipharyngioma

A

Ada: cystic, fibrotic, calcified area. Cysts ahev green-brown fluid. Cells may adhere to nearby vessels, nerves, or brain, well-circumscribed
Papillary: no cysts or calcification

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66
Q

Histology adamnatinomatous

A

Basaloid cells resting on loose connective tissue surrounding lobules of well-differentiated squamous epithelial cells. Nodules of keratin and cysts with debri.

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67
Q

Histology papillary cranipharyngioma

A

Well-differentiated squamous, no basaloid layer or nodules of keratin

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68
Q

Genetics adamnatinomatous

A

b-catenin

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69
Q

Most common glioma in children

A

Pilcytic astrocytoma

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70
Q

Where are pilocytic astrocytomas found?

A

Throughout CNS (brain, nerves, hypothal, stem, etc)

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71
Q

Signs of pilocytic astrocytoma

A

Headache, nausea, vomiting, clumsiness (cerebellar), loss of vision (ootic), hemiparesis (thalamic), hypo/pit dysfuncion (hypo)

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72
Q

Gross pilocystic astrocytoma

A

Well-demarcated, soft, tan-gray, sytic, contract-enhancing, slow-growing

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73
Q

Packed bipolar astrocytes adjacent to short stellate astrocytes. Rosenthal fibers, eosinophilic granular bodies.

A

Pilocytic astrocytomas

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74
Q

Genetics of pilocytic astrocytomas

A

NF-1 (esp optic), loss of 17q (sporadic)

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75
Q

Rathke’s cleft cyst composition

A

Single layer of columnar epithelium (may be goblet or cilliated) on layer of collagenous connective tissue. Cells produce watery or mucoid material.

76
Q

Treatment of Rathke’s cleft cyst

A

Surgery, but 15% recurrence

77
Q

Signs of Rathke’s cyst

A

Mostly incidental, if in suprasellar (>1 cm) visual, endocrine, diabetes insipidus

78
Q

What is lymphocytic hypophysitis?

A

Autoimmune disorder that causes pituitary insufficiency

79
Q

Epidemiology lymphocytic hypophysitis

A

Women in late pregnancy or after delivry

80
Q

Gross & microscopic lymphocytic hypophysitis

A

Firm, infiltrated by T and B lymphocytes, plasma cells, histiocytes. +/- follicles w/germinal centers.

81
Q

Infiltrates may spread to other endocrine organs liek the thyroid or adrenal glands, antibodies to pituitary tissue and/or hormones

A

Lymphocytic hypophysitis

82
Q

ADA criteria for DM

A

Fasting > 126
Random > 200 (w/classic symtoms)
HBA1c >6.5%
Load >200 (2 hrs after 75 g)

83
Q

What can falsely elevate HBA1c levels?

A

Prolonged RBC life

84
Q

What can falsely lower HBA1c levels?

A

Decreased RBC life: pregnancy, anemia

85
Q

Pre-diabetes criteria

A

Fasting - 100-125
Load - 140-199
HBA1c - 5.7-6.4

86
Q

How is glucose sensed by beta cells?

A

GLUT2

high Km glucose transporter

87
Q

What is the role of glucokinase?

A

Traps glucose in beta cells by converting it to G6P

88
Q

Delta cells in the pancreas secrete

A

Somatostatin

89
Q

Alpha cells in the pancreas secrete ____ and are located in ______

A

Glucagon

Periphery

90
Q

Which cells are closest to the arterioles in the center of a pancreatic islet?

A

Beta cells

91
Q

How is glucagon secretion mediated?

A

Beta cells sense glucose. High glucose will cause release of insulin, which will spread to alpha cells and inhibit release of glucagon.

92
Q

Describe the pathway of insulin secretion from the beta cell

A

Glucose enters through GLUT2, glucokinase turns it to G6P, ATP is formed through glycolysis, ATP inhibits ATP-sensitive K channel, membrane is depolarized, voltage-dependent Ca channels open, insulin storage granules released

93
Q

Which enzyme cleaves the insulin preprohormone into alpha and beta chains and c-peptide?

A

carboxypeptidase

94
Q

Which phase of insulin secretion is first lost in diabetes?

A

The first phase (10 min after a meal)

95
Q

Amylin

A
  • Co-secreted from beta cell with insulin
  • suppreses glucagon, slows gastric emptying, promotes satiety
  • reduced or absent in DM
96
Q

Insulin effects on glucose uptake

A

Increase uptake in muscle and fat (GLUT-1/4) but not liver (insulin-independent, more taken up by liver when insulin-deificient)

97
Q

Insulin effects on glucose storage and release

A

(-) hepatic gluconeogenesis [PEPCK]
(-) glycogenolysis [glyc phosphorylase]
(+) glycogen synthesis [glyc synthase]

98
Q

Insulin effects on FA synthesis and storage

A 
(-) lipolysis in adipocytes [HSL]
(-) FA oxidation [malonyl CoA blocks CPT1]
(+) TG-->FFA [LPL]
(+) FFA-->TG inside fat cells
(+) FA synthesis [FA synthase]
99
Q

Insulin effects on protein synthesis and storage

A

(+) translation factors and elongation factors

(-) of protein catabolism

100
Q

Which is the onyl hormone that protects against hyperglycemia?

A

insulin

101
Q

What is the first defense to protect against hypoglycemia?

A

Reduced insulin secretion.

Low insulin: + hepatic output, - muscle/fat utilization

102
Q

How does glucagon protect against hypoglycemia?

A

More hepatic output (+glycogenolysis, +gluconeogenesis)

103
Q

How to catelcholamines protect against hypoglycemia?

A

Stilumate B2 (+hep output), less utilization in muscle, mobilization of lactate and alanine from muscle & glycerol from fat (gluconeogenic),stimulate a2 receptors to release insulin

104
Q

Which hormone is mainly responsible for symptoms of hypoglycemia?

A

Epinephrine

105
Q

How does GH protect against hypoglycemia?

A

ketone production from released of FA, more hepatic output, less important that other hormones

106
Q

How does preganncy affect the HBA1c test?

A

Underestimates

107
Q

How does low insulin affect glucose levels?

A

Increase
More uptake in liver, but not make into glycogen for storage. More glucose made and glycogen broken down because of counter-regulatory hormones, since tissues believe there is glucose shortage.

108
Q

How does low insulin affect lipids metabolism?

A

Increased levels in blood
Less synthesis/storage and more lipolysis and mobilization. Oxidation in mitochondria = ketones. DKA or HHS (high glucose)

109
Q

How does low insulin affect protein?

A

amino acid production

Increased gluconeogenesis and urea production, azoturia (protein in urine)

110
Q

Which HLA is associated with T1D?

A

DR/DQ

111
Q

T1D patients can have autoantibodies to what?

A 
AI-2 (insulinoma-associated antigen-2)
AI-2b (AI-2 homologous antigen)
GAD65 (glutamic acid decarboxylase)
ICA (cytoplasmic islet cell)
IAA (insulin)
112
Q

Autoimmune destruction of beta cells in T1D is mediated by which cell type?

A

T cells

113
Q

What is LADA?

A

Latent autoimmune diabetes of adulthood

Less severe T1D that won’t present until adulthood

114
Q

What is Type 1a diabetes?

A

Autoimmune type 1 diabetes

115
Q

What is type 1b diabetes?

A

Idiopathic diabetes

116
Q

What are the typical things associated with idiopathic diabetes?

A

Mild DKA but no autoimmune markers, obesity with weight loss.

117
Q

How are idiopathic diabetes patients treated?

A

At first, need high dose insulin, can be switched to oral atgents later on. insulin requirements tend to wax and wane.

118
Q

Why do patients with T2D get polyuria and polydypsia?

A

Blood glucose exceeds kidney’s absorbing capacity (osmotic diuresis), free water loss and increased thrist.

119
Q

What is acanthosis nigricans?

A

Thickening and hyperpigmentation of skin folds typically associated with insulin resistance

120
Q

What occurs first, macrovesicular complications or microvesicular complications?

A

Macrovesiclular first (atherosclerosis and peripheral vascualr disease)

121
Q

What is MODY?

A

Maturity onset diabetes of the young, inherited AD, nonketotic, under 25 yrs, no obeses or resistant, defect in b-cell function (ex: glucokinase)

122
Q

What are some complication of maternal diabetes?

A

preeclampsia, polyhydramnios, infections, stillbirthm, macrossomia, neonatal hypoglycemia

123
Q

3 microvascular complications of diabetes

A
  • diabetic retinopathy
  • renal disease
  • neuropathy
124
Q

3 macrovascular complications of diabetes

A
  • Heart disease
  • stroke
  • ED
125
Q

Risk factors for developing complications of diabetes

A

Duration, hyperglycemia, HTN, genetics, smoking, compliance

126
Q

HBA1c is an estimate of glucose control for the past _____

A

3 months

127
Q

T or F: Patients with comorbidities should be on stricter glucose control

A

False. Those with hypo, age, or heart disease have a goal of 7.5-8% instead of 6-6.5%.

128
Q

Kussmaul respirations are a sign of

A

DKA

129
Q

What is the teatment for DKA?

A

Saline and insulin drip

130
Q

DKA is considered resolved if gluc under ____, venous pH ____ and anion gap _____

A

Gluc 7.3, AG < 12

131
Q

What are the characteristics of non-proliferative diabetic retinopathy?

A
  • microaneurysms (dot & blot)
  • exudates (hard & sharp from lipoproteins, edema)
  • macular edema (thickening of retina)
  • retinal ischemia (cotton-wool spots, venous beading)
132
Q

What is the first finding in diabetic retinopathy?

A

Microaneurysms

133
Q

What 3 findings suggest pre-proliferative retinopathy>

A

IRMA (intra=retinal microvascular abnormalities), venous bleeding, intra-retinal hemorrhages

134
Q

What are the characteristics of proliferative retinopathy?

A
  • neovascularization
  • fibrosis (contract=detachment)
  • Vitreous hemmorhage
  • Traction retinal detachment
135
Q

Where is neovascularization retinopathy usually found?

A

Near optic nerve head and surface (outer layer) of retina

136
Q

2 risk factors apart from glucose control that predisposes to retinopathy

A
  • Duration of disease

- Ethnic (mexicans)

137
Q

Risk factors for retinopathy

A

Duration, hyper, genetic, HTN (diastolic over 70), puberty, nephropathy, smoking, pregnancy

138
Q

When should Type 1 diabetics get first eye exam?

A

3-5 yrs (initial after diagnosis)

139
Q

How often should diabetics get eye exams?

A
  • Annual (children, adult w/out retinopathy)
  • Semi (non-proliferative)
  • Quarter (Pre-proliferative)
  • Individual (Proliferative)
140
Q

What is diagnostic of early stage renal disease?

A

Microalbuminuria (2/3 samples in 6 mo)

- 20-200 ug/min or Alb/Cr ratio

141
Q

What are some treatments of early diabetic nephropathy?

A
  • glycemic control
  • ACEI or ARB (ALWAYS X pregnancy)
  • Low protein diet
  • Aldose reductase inh (exp)
  • PKC inh (exp)
142
Q

Risk factors for diabetic neuropathy

A
  • genetics
  • male
  • tall
  • alcohol
  • hyperlgycemia
143
Q

Vibratory perception measure __ nerves

A

Large

144
Q

Thermal perception measure __ nerves

A

Small

145
Q

How can you tell if someone has a pseudocushing state?

A

Gluccocorticoid excess but diurnal rhythm is intact

146
Q

What is the cosyntropin test used for?

A

ACTH analog used to stimulate production of cortisol. Diagnosis of primary adrenal insufficiency if no cortisol increase.

147
Q

What is the metyrapone test?

A

CYP11B1-OHase inhibitor. Give at night, 11-deoxycortisol should be high in morning (loss of feedback inhibition). Checks secondary adrenal insufficiency

148
Q

How can you test for 2ry adrenal insufficiency?

A
  • insulin (cortisol peak normal)
  • metyrapone (11-deoxycortisol in morning normal)
  • cosyntropin (pass standard but fail low dose)
  • DHEA-S (normal excludes acquired deficiency)
149
Q

What is Conn’s disease?

A

Excess aldosterone

150
Q

What are the clinical features of mineralicorticoid excess?

A
  • HTN (resistant, <40 yrs)
  • hypokalemia
  • met alkalosis
  • hypomagnesemia
  • no edema
151
Q

What caused apparent mineralicorticoid excess syndrome?

A

11b-HSD2 deficiency. Cortisol activates MR. Also can occur with licorice and carbenoxolone.

152
Q

Familial hyperaldosteronism is due to what gene?

A

Fusion protein from linked CYP11B1 and CYP11B2

153
Q

How to diagnose Liddle syndrome

A

Mineralocorticoid excess responds to amiloride but not spirinolactone. (Apical ENaC constitutively active)

154
Q

What is the mechanism behind pregnancy-induced HTN?

A

Mutations in MR allow progesterone to act as agonist

155
Q

Which conditions can cause mineralocorticoid excess?

A
  • 1ry or 2ry adosteronism
  • DOC excess (tumor)
  • 11/17-hydroxylase insuff
  • GGI (21-hydroxylase + HTN/hyerK)
  • AME
  • Liddle’s
156
Q

How to screen for aldo excess

A
  • 24 hr Urine: K >30meq and Na >100meq

- Plasma renin/aldo ratio

157
Q

How to confirm adlo excess

A
  • 24 hr urine @ high salt w/no aldo suppresion
  • Saline influsion w/no aldo supp.
  • Fludocortisone test w/high urine aldo
158
Q

What are the localizing studies used for hyperaldo?

A

Adrenal CT (tumors) or adrenal vein sampling (unilateral tumor)

159
Q

What are some signs of primary adrenal insufficiency?

A

Weakness, weight loss, nausea, hyperpigmentation, hypotension, hyponatremia, hyperkalemia

160
Q

What medications must you stop before screening for hyperaldo?

A

Discontinue ACEI, ARBs, diuretics, NSAIDS.

Can use alpha blockers and low dose beta blockers

161
Q

How do you treat mineralocorticoid excess?

A

Surgery or spirinolactone

162
Q

Which disorder causes salt wasting with normal glucocorticoid activity?

A

Aldo synthase (CYP11B1) deficiency

163
Q

Why is secondary adrenal insufficiency usually limited to gluccocorticoids?

A

Mineralocorticoids are not dependent on ACTH

164
Q

Intra-adrenal pheochromocytomas usually make

A

epinephrine (except VHL)

165
Q

Extra-adrenal pheochromocytomas (apargangliomas) usually make

A

NE

166
Q

Glomus tumors of head and neck usually make

A

dopamine

167
Q

What is COMT? Where is it found? Why is it important?

A

Catechol O-methyl transferase. Present in periphery and convert catelcholamines to metanephrines. Tumors usually contain it (easier to diagnose)

168
Q

What enzyme is needed to amke HVA & VMA from metanephrines?

A

MAO

169
Q

What are the 5 P’s of pheochromocytoma?

Other symptoms?

A
  • Pressure (spikes & elevation)
  • Pain (acute throbbing headache)
  • Perspiration (drenching)
  • Pallor (minimal exertion)
  • Peripheral vasoconstriction
  • orthostasis, hyperglyc, hypercal, tremor
170
Q

MEN-2A is susually associated with

A

MTC, hyperPTH, RET mutations

171
Q

MEN-2B is ususally associated with

A

MTC, marfanoid habitus, musocsal neuromas, RET mutations

172
Q

How to diagnose pheochromocytoma

A
  • collect 24 hr urine to measure cate & meta & Cr
  • positive if excretion 2X above upper limit normal
    OR
  • collect plasma meta in calm conditions
  • elevation in meta positive (slightly elevated normeta is common)
173
Q

Which medications/conditions can cause false positives in pheo diagnossis?

A
  • sleep apnea
  • clonidine use/withdrawal
  • tricyclic antidepressants
  • MEN or VHL presymptomatic states
174
Q

How to prepare for pheo surgery

A
  1. a1 blockade (until stuffy)
  2. 2 weeks salt overload
  3. Tyrosine hydroxylase inhibitor (block syntehsis of catecholamines)
  4. b2 blockers
175
Q

What to do in incidental adrenal nodule is found

A
  1. Check BP and K
  2. Screen for Cushings and Pheo if HTN/hypoK
  3. If nasty-looking, biopsy if Pheo is neg
  4. Hounsfield units 3 cm, monitor (scan 6 mo)
  5. > 4 cm, remove
176
Q

The pituitary fossa is bound anteriorly and inferiorly by

A

sphenoid sinus

177
Q

The pituitary fossa is bound posteriorly by

A

bony dorsum sella

178
Q

The pituitary fossa is bound laterally by

A 
Cavernous sinuses
(internal carotid a, CN 3/4/6, 1st two divisions of 5)
179
Q

The pituitary fossa is bound superiorly by

A

Diaphragma sella

optich chiasma within suprasellar cistern

180
Q

Eosinophilic adenomas secrete

A

GH

181
Q

Basophilic adenomas secrete

A

ACTH

182
Q

What is a pituitary apoplexy/

A

Infarction of a pituitary adenoma causing acute swelling of the tumor and hemorrhage

183
Q

How do you treat a pituitary adenoma that is secreting over 200 ng/mL of prolactin?

A

Dopamine agonists (bromocriptine and cabergoline)

184
Q

How do you treat a pitoma which is mainly secreting GH?

A

Surgery

Radiation or medication if surgery not possible

185
Q

How do you treat a pitoma which is mainly secreting ACTH

A

Surgery

radiation or medication if surgery not possible

186
Q

Which surgical method cannot eb used for predominantly suprasellar tumors?

A

Transphenoidal (need to use transcranial approach)

Endo & Repro block (2 decks)

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