Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Pancreas And Adrenals > Flashcards

Pancreas And Adrenals Flashcards

1
Q

Endocrine pancreas

A

Actress vasculature andsend to target organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Islet of langerhans

A

Discrete collection of small blue islands in neck and tail of pancrease

Very vascular bc endocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PP celll

A

Secrete pancreatic polypeptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

D1cell

A

Secrete VIP:vasoactive intestinal polypeptide

Rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glucose homeostasis

A

Regulating insulin and glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glucagon

A

Mobiliza glucose primarily from liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Insulin receptor

A

RTK MEK to MAP kinase

rek PI3K AKT

Both increase glycogen lipid/protein synthesis
Decreases lipolysis
Cel growth and differentiation** anabolic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

C peptide

A

Proinsulin is cleaved toform insulin and c peptide

C peptide is a marker of endogenous insulin
-can differentiate from insulin administrations as a pharmaceutical agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Incretins

A

Oral*** glucose stimulated release of GLP-1 and GIP

Which go straight to pancreas for early onset insulin release and inhibitit glucagon and glucose production

Early and potent recognize blood sugar will go up and early insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MOA incretins

A

Stimulate insulin release and inhibit glucagon release resulting in lower blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Inactivation incretins

A

Dipeptidyl peptidase-4 DPP4

*drugs ending in glipton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diabetes mellitus

A

Defective insulin secretion or effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

A1c

A

> 6.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

FPG

A

> 126

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

OGTTT

A

> 200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

RPG

A

> 200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Asians

A

Low diabetes but if break out south asians (high)

East Asian 9low )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ASian Indians

A

High as African Americans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Type 2 diabetes in kids under 20

A

10-19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Type 1 diabetes age

A

1-19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Who gets type 2 diabetes

A

More likely in teenage population than type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Onset type 1and 2

A

1-childhood and

2-increasing in childhood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Type 1 and 2 cause

A

1-autoimmune T. Cell selection and regulation leading to breakdown and self tolerance

2-insulin resistance in peripheral start (no autoantibodies ) but increasing in adolescents!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pathology

A

Insulitis and autoantibodies present (inflammatory infiltrate) B cell depletion and islet atrophy

2-no insulinitis; amyloid depositio in islets mild B cell depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Type 1 histology

A

Failure of T cell self tolerance-see t lymphocytes directed against antigens on the pancreativ beta cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MHCII type I

A

6p21 for 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Development of type 1

A

Lack of insulin from immune destruction of islet cells. Must be over 90% destroyed to give overt symptoms

Only occurs when mass is 10% of normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Type 2 diabetes

A

Insulin resistance and B cell dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why are they resistant to insulin

A

Obesity

Metabolism of adipose tissue cause FFA which are toxic and go into cell and disrupt insulin pathway.

Adipokines-some protective some negate insulin effect(these are elaborated when excess adipose tissue is present)

Inflammation -damages cells targeted and pancrease itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Insulin resistance over time

A

Secretion increases initially to compensate

Then decreased wear out and give T2DMD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Genetics T2DM

A

More likely to have first degree relative with T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

As lose insulin

A

Get islet B cell failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What has to be present to T2DM to cause symptoms

A

Beta cell dysfunction!!!

Beta cells are exhausted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

MODY

A

Onset childhood, nonketo, increased blood insulin but no islet antibodies

Monogenic——from mutation inhibiting glucokinase

Not autoimmune not insunilnitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Gestational diabetes

A

Pregnancy promotes a hormonal state with diabetogenic properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Risk gestational diabetes to mom

A

C section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Ribs to fetus

A

Neonatal hypoglycemia->seizures->brain damage

Macrosomia

Congenital malformation

Stillbirth

***screen for it!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

First prenatal visit

A

Measure FPG, HBA1c or random plasma glucose
>6.5
>126
>200

Treat and follow up as for preexisting diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

24-28 week screen that passed first

A

OGTT in morning after overnight fast

Fasting >92
1 hour after >180
2 hour >153
Have it and treated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

T1 and T2

A

Hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Triad of T1

A

Polyphagia, polyuria, polydipsia

Severe-ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

T2 clinical

A

Fatigue, vision changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

4 T in kids t1D

A

Toilet-glucose pulls fluid from tissue osmotic
Thirsty-glucose pulls fluid from tissue
Tired -lack of sugar in cells!!
Thinner-without energy sugars supply lose weight
Hunger-without glucose need more food

Fruity breath-keno from burning fat instead of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Young kid brought in is it type 1 or 2? How tell? What test?

A

Autoantibodies in caucasion More reliable in caucasion for type 1 . But if have autoantibodies out there then type 1. Harder to tell if not caucasion

HLA DR/DQ on chomosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Diabetic ketoacidosis

A

Type 1, severe acute diabetic complication

Can be presenting feature of T1DM in adult and kid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Why get DKA if have diabetes

A

Non compliance

Precursor infection-pneumonia, UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Triad of ketoacidosis

A

Hyperglycemia, ketonemia, metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why get ketoacidosis

A

Effect of hyperepinephric state (not using glucose so get glucagon for gluconeogenesis and insulin defiency proton FFA release)
Kidney dumping ketones and osmotic diuresis so dehydrated

SHOCK, DEHYDRATION: secrete more epinephrine so spiral over and over

EPINEPHRINE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Accumulate ketones

A

Acetoacetic acid and beta hydroxybutarate in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

DKA

A

Hyperglycemia, ketonemia and acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Resulting in

A

Dehydration, polydipsia, polyuria/ketouria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Presenting signs

A

Nausea/ vomiting, tachycardia, kussmal respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What do to help metabolic acidosis

A

Respiratory kussmall respiration breathing a lot blowing CO2 off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Treat DKA

A

Insulin, hydration, potassium!!

All hypokalemia even if K high!!
Usually in RBC but when insulin drop K leave cells and treat with insulin K back into cells so always hypokalemia so moment give insulin need to be ready to treat with K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Hyperglycemia hyperosmotic syndrome

A

Acute hyperglycemia crisis in T2DM.

Culmination of prolonged insulin defiency

  • increased gluconeogenesis
  • decreased glucose uptake in peripheral tissues

B cells not making insulin very hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Who more hyperglycemia DKA or HHS

A

HHS

8T1 shunt to ketogenic these patients elaborate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Presenting HSS

A

Glucose>500
Severe dehydration
Hyperosmolarity >350-> obtundation, coma
Impaired renal function

Older person in facilitated care facility and cant take care and worse control of diabetes become stuporous and spiral out of control and can be comatose when come to attention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Ketones in HSS

A

NOOOOOO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

DKS vs HHS pH

A

<73

>7,3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Osmolality DKA HHS

A

<320, >320

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Hyperglycemia DKA HHS

A

> 250 >600

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Ketones DKA HHS

A

Present, rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

DKA

A

Anion gap acidosis
Ketonemia
Ketouria
Hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

HHS

A

Hyperglycemia
High osmolality
Dehydration
Altered mental status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

HA1C

A

Glucose fasten to RBC =irreversibly glycosylation of the hemoglobin A1C—-determines for past month

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Major complications of diabetes

A

Microvascular and macrovascular , lower extremity gangrene, neuropathy (microvasular complication-why extremity disease is so bad don’t know when cut foot or when there’s an infection)

*most common cause of death in diabetics: MI

67
Q

Most common cause of death in diabetics

A

MI

68
Q

Chronic hyperglycemia causes

A

Stroke, MI, lower extremity gangrene

69
Q

Neuropathy

A

Might be having heart attack but manifest heart burn or something

70
Q

Advanced glaciated end products

A

Effect gene expression and protein function
-cytokines (TGFB and VEGF)and growth factors elaborated, ROS , procoagulant activity, cross linking of matrix proteins -proarthegenic

71
Q

End stage renal disease

A

Usually from diabetes, screen with albumin and urine

-direct damage to glomeruli, renal vascular lesions, arteriosclerosis, pyelonephritis

72
Q

Glomeruli diabetes

A

Kimmelsteil wilson nodule -matriculates in glomeruli(PAS stain pink nodules)

Thick basement membrane-

73
Q

Diabetic nephropathy

A

Urine albumin tests

Macroalbumin->300
Microalbumin-small amount 30-300

Nephropathy!losing function

74
Q

Diabetic retinopathy

A

Hemorrhages , aneurysms, cotton spots, abnormal growth of blood vessels, hypoxia, blindness

Other-cataracts, glaucoma

75
Q

Other eye complications

A

Cataracts, glaucoma

76
Q

Neuropathy

A

Peripheral, autonomic, diabetic mononeuropathy

77
Q

Decreased immune response diabetes

A

Cellulitis, pneumonia, pyelonephritis

78
Q

Pancreatic neuroendocrine tumor

A

Gross appearance yellow tan

Predilection for pancreatic neuroendocrine tumors

EM-secretory granules

79
Q

Insulinoma

A

Amyloid ***
Small and secretes lot of insulin

C peptide levels can make the diagnosis

Hypoglycemia and insulin levels high!!
Then check c peptide levels
C peptide increased

80
Q

Gastrin OA

A

Zollinger ellison

Triad-islet cel tumor, gastric acid hypersecretion, peptic ulceration not responding to therapy for peptid ulcer think of gastrinoma HYPERSECRETION OF GASTRIC ACID AND HYPERSECRETION

Ulcers do not respond to conventional therapy
-clue to clinical diagnosis

81
Q

Somatostainoma

A

Diabetes, cholelithiasis, steatorrhea->hard to diagnose

Somatostatin functions as a paracrine regulator, so manifestations are typically inhibitory

  • reduced insulin
  • reduced gallbladder motility
  • reduced exocrine pancreatic secretions
82
Q

When somatotstatinoma come to attention

A

Bit later, but at time a lot are metastatic !

83
Q

Glucagonoma

A

Mild diabetes

Rash-necrolytic migratory erythema
-groin, lower extremities

4D
-diabetes, dermatitis, depression, DVT

84
Q

Necrolytic migratory erythema

A

Pathogenomic rash consisting of erythema with superficial areas of spideamla necrosis, progressing to epidermal shedding, bullae formation, and crushsted erosions

85
Q

VIPoma

A

Vasoactive intestinal pepdide:D1 cells

WDHA syndrome
Watery diarrhea, hypokalemia, achlorhydria

20% of patients will have flushing as well -what else gives you flushing and diarrhea

86
Q

Flushing diarrhea

A

VIPoma or carcinoid

Look at K

87
Q

Adrenal gland

A

Cortical and medullary zone

88
Q

Cushing primary

A

High cortisol and low ACTH CRH

Obesity, striae, rounded face
ACTH dependent or independent

89
Q

Adrenal gland and external stimuli

A

Very sensitive t being changed

Doing job of adrenals for them as shrink appear atrophic

ACTH dependent like cushing disease (adenoma) bilaterally hyperplastic

90
Q

Primary adenoma of adrenals cortical

A

Hyperfunction benign come to attention bc hyperfunction

91
Q

Adrenal cortical carcinoma

A

Larger! Weight >200

More likely symptomatic bc of how big they get ..very important clue

92
Q

Hypercortisolism work up

A

Check ACTH

Low-adrenals for primary conditions

High pituitary or something

93
Q

Primary hyperadrenalism

A

Elevated cortisol and corticotropin levels suppressed

94
Q

Primary hyperaldosteronism (conns syndrome)

A 
Hypertension
0refractoru HTN
-adrenal mass and HTN
-htn in young
-severe HTN (>160/100 mmHg)

Hypokalemia

Hypomagnesia

95
Q

Causes of conn

A

Most common is
Second adenoma
Familial-glomeruloasa cells respond

96
Q

Conn increased what

A

ALDOSTERONISM

97
Q

Secondary hyperaldosteronism

A

Increased RAAS

-diuretic use, decreased renal perfusion, arterial hypovolemia, pregnancy, renin secreting tumors

98
Q

Aldosterone secreting adenoma

A

Small
Young 30-40
Spironolactone bodies
High incidence of ischemic heart disase

See adrenocortical cells and spironolactone bodies-pink concretions see not sure bc tend to see if patient is treated with spironolactone with surgery

99
Q

Why use spironolactone aldosterone secreting adenoma

A

Spironolactone so get spironolactone bodies ,

100
Q

HTN to ischemic heart disease in 30-40

A

Aldosterone secreting adenoma-primary hyperaldosteronism

101
Q

How tell primary vs secondary hyperaldosterone

A

Plasma renin high in secondary low in primary (adrenal CT and adrenal vein sampling!)

102
Q

Adrenogenital syndromes

A

Virilization

And congenital adrenal hyperplasia

103
Q

Pituitary adrenogenital syndromes

A

ACTH stimulate androgens-cushing

104
Q

Adrenal adrenogenital syndromes

A

Primary adrenal neoplasm
-adenoma, carcinoma (more common)

Carcinoma is virilizing

105
Q

CAH

A

Inherited error of metabolism
-AR

Defective enzyme responsible for steroidogenic is

Impaired feedback to hypothalamus/pituitary, with resultant hyperplasia

90-95% caused by defiency of 21-hydroxylase

106
Q

Decrease glucocorticoids CAH

A

ACTH up and go and make adrenal big! But last thing to occur really…

107
Q

Most common CAH

A

21 hydroxylase defiency

108
Q

Salt wasting of 21 hydroxylase

A

No mineralocorticoids or cortisol

109
Q

Male and femal infants 21 hydroxylase

A

Salt wasting->hyponatremia
Hyperkalemia
Hypotension

In first weeks of life

110
Q

Why females better for 21 hydroxylase

A

Can tell at birth when virilized

111
Q

Long term 21 hydroxylase defiency

A

Adrenomedullary dysplasia: hypotension

112
Q

What see with virilization

A

Fused labia and large clitoris and scrotal appearance of labia

113
Q

Partial lack of 21 hydroxylase

A

Simple virilizing syndrome (without salt wasting

114
Q

What have in simple virilization

A

Some mineralocorticoids and small amount of cortisol, not enough to prevent ACTH

115
Q

Non classical late onset adrenal virilsm

A

Most common

Partial lack

  • precocious puberty
  • acne and hirsutism at time of puberty
116
Q

Diagnose CAH

A

Serum 17 hydroxyprogesterone

ACTH stimulates test

117
Q

Treat CAH

A

Glucocorticoids

  • replenishes cortisol
  • provides negative feedback for ACTH suppression
  • no further overstimulation of androgen production

Mineralocorticoids as necessary

118
Q

Adrenocortical insuffiency

A

Primary insuffiency
-loss of cortical cells, defect in homogenous

Secondary insuffiency
0hypothalamic-pituitary disease
-BPA suppression by extra adrenal steroid use

Chronic vs acute

119
Q

Primary acute adrenocortical insuffiency

A

Adrenal crisis
Rapid withdrawal of steroids
Massive adrenal hemorrhage

Table 24-10

120
Q

Relative adrenal insuffiency patient

A

ICU for meningitis and become hypotensive and not responding to fluid replacement …something given them inadequate HPA response to situation

Not a lot of CRH, corticotrophin and decreased cortisol

ICU aren’t alert or aware so observe what’s going on this can be fatal . Hypotension leads to shock death

121
Q

Exogenous steroid withdrawal

A

Steroid administration results in suppression of acth production by the pituitary through negative feedback

If prolonged adrenal hypofunction atrophy

Rapid withdrawal of exogenous steroids results in adrenal insufficiency WHY GIVE STEROID TAPER DO NOT RAPID WITHDRAWAL

122
Q

Adrenal hemorrhage

A

Sepsis-Waterhouse friedreich Sean syndrome

Neonatal period
Trauma
Postsurgical patients
Coagulopathy

123
Q

How regocnize

A 
Hypotension
Abdominal pain
Fever
Nausea/vomiting
Hyponatremia
Hypoglycemia
124
Q

Primary chronic adrenocortical insuffiency

A

Long duration of malaise, fatigue
Anorexia and weight loss
Joint pain
Hyperpigmentation of skin

125
Q

Why hyperpigmentation adrenocortical insuffiency

A

Increase POMC from pituitary , which makes ACTH, MSH

MSH pigmentation

126
Q

Nelson syndrome

A

Out adrenals pituitary secrete more acth and HYERPIGMENTATION

127
Q

Addison

A

Primary adrenal insuffiency

-feeble heart, change in skin, languor and debility .org

128
Q

Addison autoimmune?

A

Calcification adrenal glands

T most common cause of Addison when initially described

129
Q

Primary chronic adrenocortical insuffiency

A

Most common-TB

Workwide-autoimmune

Most common in developed countries autoimmune

130
Q

Autoimmune adrenalitis

A

> 70% of all cases of primary hypoadrenalism in the western world

APS1 APS2

131
Q

APS1

A

Mutation in AIRE
-adrenalitis, parathyroiditis, hypogonadism, pernicious anemia

Mucocutaneous candidiasis (ab IL17 and IL22), ectodermal dystrophy

APECED autoimmune polyendocrine with candidiadisis and extodermal dystrophy

132
Q

Autoimmune polyendocrine syndrome

A

Adrenalitis
Thyroiditis
Type 1 diabetes

133
Q

Ectodermal dystrophy

A

Type 1

Terrible teeth and no nails..?

134
Q

Presentation adrenocortical insuffiency lack of corticosteroids

A

Malaise, NV, hypoglycemia, refractory hypotension

135
Q

Presentation of adrenocortical insuffiency lack of mineralocorticoids

A

Hyperkalemia, hyponatremia

136
Q

Test adrenocortical insuffiency

A

Random cortisol and acth stimulation test

137
Q

Adrenal metastasis

A

For carcinomas go into adrenals

138
Q

Mucus pigmentation

A

Adrenal insuffiency

139
Q

Tuberculous adrenalitis

A

Caseating granuloma multinucleated giant cell

Sheet of necrosis tuberculous adrenalitis

140
Q

Autoimmune adrenalitis

A

Influx of lymphocytes bc autoimmune

141
Q

Adrenal cortical neoplasia

A

Adenoma and carcinoma

142
Q

Adenoma

A

Incidental on radiography

Functional

143
Q

Carcinomas

A

Incidental on radiography
Functional
***Compression/invasion of adjacent structures virilizing

Can hemorrhage into self and present acutely PAINFUL if bleedinto self

144
Q

Carcinoma vs adenoma

A

Size HUGE predictor to adrenal cortex

Adenoma small
Carcinoma huge 300grams

145
Q

Adrenal medulla

A

Centrally located chromaffin cells

Responsible for catecholamines

Same as paraganglionic stuff

Sympathetic control

146
Q

Histology adrenal medulla

A

Nests of endocrine cells when form tumors that’s what look like

147
Q

Pheochromocytoma

A

HTN!
From catecholamines secretin from the tumor
10% rule
-10% are extra adrenal (paraganglioma), 10% bilateral, 10% in kids, 10% malignant, 10% not associated with HTN

25% rule
25% familial

148
Q

How tell pheochromocytoma malignant

A

Metastasis

149
Q

HTN with pheochromocytoma

A

> 90%

HA, palpitations, diaphoresis*** (sweating) all from catecholamines release

Acute-catecholamines
Chronic cardiomyopathy

150
Q

Chronic pheochromocytoma

A

Cardiomyopathy

151
Q

Test pheochromocytoma

A

Urine and plasma metanephrines

152
Q

Myelolipoa

A

Benign fat and bone marrow, vary in size, can present with hemorrhage

May bleed into self and give pain

153
Q

Adrenal incidentalomas

A

> 4 cm ..size matters (less than 4 adenoma)

Positive functional assays

  • dexamethasone suppression test for hypercortisolism
  • pheochromocytoma
  • this checks for adenoma

CT enhancement characteristics

154
Q

MEN1 gene

A

Men1 menin tumor suppressor gene

155
Q

3 P of MEN1

A

Primary hyperparathyroidism

Pancreatic endocrine tumor-insulinoma and gastrinoma

Pituitary adenoma-lactotroph and somatotroph

May also get duodenal gastrinoma

156
Q

Type 2A gene

A

Germline gain of function mutation in RET Porto oncogene

157
Q

Tumors of MEN2a

A

Medullary thyroid carcinoma
Parathyroid hyperplasia

Pheochromocytoma

158
Q

Type 2B gene

A

Germline gain of function utation in RET protooncogene

159
Q

Tumors 2B

A

Medullary thyroid carcinoma

Pheochromocytoma

Mucosal neuromas

160
Q

Familial medulary thyroid carcinoma General

-just one not multiple

A

Germline gain of function RET protooncogene oncogene

161
Q

MEN physical 2B and

A

Marfan and can be cloud

162
Q

Generalities of MEN

A

Patients develop tumors at younger ages

More likely to be b/l and multiple

Preceding hyperplasia is often seen

Tumors tend to be aggressive and recurrent

163
Q

Pineal gland

A

Third eye-comprised of photoreceptor containing neural tissue

Melatonin secretion

164
Q

Tumors of pineal gland

A

Germ cell tumors
Pineocytoma
Pineoblastoma

Pathology (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions