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Hannah Endo/Repro year 2 > Endo- endocrine pancreas pathology > Flashcards

Endo- endocrine pancreas pathology Flashcards

1
Q

risks to mom and fetus of gestational DM

A

mom: C-section
Fetus: macrosomia, congenital malformations, still birth, neonatal hypoglycemia–> seizures–> permanent brain damage

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2
Q

how is T2DM usually found

A 
on screening 
(chronic slow onset begins with changes in vision and fatigue)
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3
Q

pH, bicarbonate, anion gap, osmolality, hyperglycemia, and ketones in DKA vs HHS

A

DKA:

  • pH: <7.3
  • bicarb: <18
  • anion gap: >10
  • osm: <320
  • hyperglycemia: >250
  • ketones present in blood and urine

HHS:

  • pH: >7.3
  • bicarb: >18
  • anion gap: variable
  • osm: >320
  • hyperglycemia: >600 (extreme)
  • ketones absent in blood/urine
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4
Q

Most common cause of death in diabetics

A

myocardial infarction

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5
Q

classic triad of DKA? other sx? most common underlying etiology of DKA ? others?

A

triad: hyperglycemia, ketonemia, metabolic acidosis
(D- diabetic, K-ketonemia, A-acidosis)

other: dehydration, shock, polydipsia, polyuria/ketouria, —-> N/V, tachycardia, Kussmaul Respirations (respiratory effect of acidosis trying to compensate by trying to elicit respiratory alkalosis)

MC: non-compliance

others: precursor infection (pneumonia, UTI)

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6
Q

classification of T1DM vs T2DM (onset, Ab status, pathogenesis, and pathology)

A

T1DM

onset: usually childhood/adolescence
- Circulating islet autoantibodies (anti-insulin, anti- GAD, anti-ICA512)
- pathogensis: dysfunction of in T cell selection and regulation leading to breakdown in self-tolerance to islet autoantigens (Tcells fight beta cells)
- pathology: insulitis (inflammatory infiltrate of T cells and MOs), Beta cell depletion, islet atrophy

T2DM

onset: usually adult but can occur in children
- no islet Ab
- pathogenesis: insulin resistance in peripheral tissues, failure of compensation by beta cells
- pathology: no insulitis, amyloid deposition in islets, only mild B-cell depletion

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7
Q

how to screen for diabetic nephropathy ?

A
  1. screen
    albumin: creatine ratio in urine
    * gold standard for urine albumin testing = UACR (urine albumin: Cr ratio)
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8
Q

define the gastrinoma triad . dx?

A

(ZES)

triad: islet cell tumor (G cells) ; gastric acid hyper secretion; peptic ulceration (esp in duodenum)
* *PUD signs and sx that do not response to NL tx

  • patients can present with free air in abdomen on CT due to perforated gastric ulcer
  • like to metasize to liver

dx: + secretin test, + calcium infusion test

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9
Q

classic triad of T1DM ? other sx? complications?

A

polyphagia
polyuria
polydipsia

  • weight loss, fatigue, irritability, fruit smelling breath (ketones)
  • severe: DKA (intimal presentation in 20% of T1DMs)
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10
Q

3 primary pathologic lesions leading to diabetic nephropathy

A
  1. glomerular sclerosis (MC)
    - thickened BM, disrupted protein cross-linkage and filter function, progressive leak of large molecules (proteins) in urine
  2. renal vascular lesions
    - arteriosclerosis –> constriction of vessel lumen–> ischemia/ischemic damage
  3. pylenophritis
    - constant inflammation from recurrent infections
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11
Q

define features of insulinoma ? how to dx?

A
  1. small tumors (<2cm) of B cells that can produce episodes of symptomatic hypoglycemia (<50)
    * *clinical ft HYPOGLYCEMIA
    * *amyloid is common histo finding
    * *dx: C-peptide levels (indicate insulin is from endogenous source vs exogenous)
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12
Q

the major risk factor for T2DM? is there a genetic component?

A

RF: obesity
genetic: yes majority have a 1 degree relative with it as well

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13
Q

cycle of DKA

A
  1. insulin deficiency promotes FFA release which generates ketones
  2. ketones build up causing ketoacidosis, and ketones are carried into the urine
  3. the excess glucose and ketones in the urine draws out water (osmotic diuresis) and causes dehydration, low BP, and shock
  4. the body release epinephrine in response to cause vasoconstriction to try and raise BP
  5. .however the dumping of glucose causes glucagon to be released, promoting gluconeogenesis
  6. the effect of epinephrine causes the body to not be able to use glucose, which cause it to accumulate in blood –> worsening hyperglycemia
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14
Q

define islet of langerhans

A

discrete clusters of endocrine cells with specific functions that make up the endocrine pancreas (alpha, delta, beta, D1, and PP cells)

  • they are vascular
  • predominate in the neck and tail of the pancreas
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15
Q

unifying features (gross, location, histo, EM) of a pancreatic neuroendocrine tumor (all of which are malignant/carcinomas) ? and types ?

A

gross: solid, tan-yellow (possible spots of hemorrhage)
location: predilection for pancreatic neck and tail
histo: well-differentiated neuroendocrine tumors
EM: secretory granules

types: insulinoma, gastrinoma, somatostatinoma, glucagonoma, VIPoma
(insulin only 10% metastatic rate; VIPoma is 80%)

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16
Q

what maintains glucose homeostasis

A
  1. hepatic release of glucose
  2. tissue utilization of glucose
  3. hormonal control of glucose by insulin and glucagon (+ others)
17
Q

pathologic changes seen in diabetic nephropathy on microscope and histology

A
  1. early BM thickening (electron microscopy)
  2. nodular mesangial matrix accumulation in the glomeruli that stains PAS positive (aka KIMMELSTIEL WILSON DZ)
    * looks like pink balls of protein in the kidney with PAS
18
Q

define hyperglycemic hyperosmotic syndrome (HHS)? sx?

A
  • acute hyperglycemic crisis in T2DM
  • caused by a culmination of prolonged insulin deficiency causing increased gluconeogenesis and decreased glucose uptake in peripheral tissues
  • sx: glucose >600; severe dehydration; impaired renal function; hyperosmolality (>350) –> obtundation, coma, altered mental status
  • **NO KETONES
19
Q

define MODY and its genetic linkage

A
  • *Maturity-Onset Diabetes of the Young
  • resembles T2DM clinically but not same thing
  • increased blood insulin
  • NO autoantibodies
  • Nonketotic
  • genetically linked-common loss of function of glucokinase (fxn is to serve as beta cell glucose sensor that controls the rate of glucose entry into the beta cell for the glycolytic pathway and increases insulin secretion as Blood glucose rises)
  • LOF causes increased BG which causes increased release of insulin
20
Q

key features of glucagonoma

A
  • alpha cell tumor
  • mild DM (bc increase glucagon in blood)
  • “4 D’s” - DM, dermatitis, depression, DVTs
  • Characteristic rash: NECROLYTIC MIGRATORY ERYTHEMA (esp in groin and LE) (epidermal necrosis, shedding, bullae (blister) formation, and white crusted erosions)
21
Q

___ is cleaved in the beta cell to form active ___ and _____ (which is a marker of endogenous insulin vs administered exogenous insulin)

A

proinsulin is cleaved to form active insulin and C-peptide

*C-peptide presence identifies the insulin came from inside the body

22
Q

what does each secrete: alpha cells? beta cells? delta cells? PP cells? D1 cells?

A

alpha: glucagon
Beta: insulin (most numerous cell in islets)
delta: somatostatin
PP: pancreatic polypeptide
D1: VIP (vasoactive intestinal polypeptide)

23
Q

is hepatic glucose output increased or decreased in T2DM

A

increased
(along with insulin resistance and decreased insulin secretion)
overall = hyperglycemia

24
Q

define HbgA1c and its use clinically

A

-irreveisble glycoslyation of the hemoglobin tetramer = HgbA1C
(comes from glucose being in the blood for a month and irreversibly binding to Hgb)
-measure of long term diabetic control since binding takes over 1 month
-target : <6.5-7 (BG < 154 avg)

25
Q

B cells must be ____ destroyed to give overt T1DM sx, before that the sx are mild

A

> 90% destroyed

26
Q

Insulin release pathway: 1. ___ transporter takes glucose up into beta cells. 2 glucose metabolism generates ___. 3. ATP inhibits ____. 4. ____ results in ___ influx that results in insulin release

A
  1. GLUT-2
  2. ATP
  3. K+ membrane channels
  4. depolarization –> Ca2+ influx
27
Q

major complications of diabetes

A

chronic hyperglycemia–>

  1. increased risk of:
    - stroke (brain)
    - MI (2x) and CAD
    - LE gangrene (100x) !!!
  2. retinopathy, cataracts, glaucoma
  3. nephropathy
  4. neuropathy
  5. increased risk of infection (cellulitis, pneumonia, pyelonephritis)
28
Q

what is the leading cause of ESRD in the US

A

diabetic nephropathy

29
Q

how to test for DKA

A
  1. test for ketones in urine (aceotoacetic acid and beta-hydroxybutyrate) confirms ketonemia
  2. blood glucose (confirms hyperglycemia)
  3. arterial blood gas (confirms acidosis)
30
Q

what three factor of obesity illicit T2DM ? how do they affect beta cells

A
  1. adipokines
    - elaborate the bad type that resist insulin
  2. FFA’s
    - toxic metabolite of adipose tissue that disrupts the insulin pathway (lipotoxcity to beta cells)
  3. Inflammation
    - causes damage to end organs inhibiting their ability to uptake glucose

*all 3 factors lead to insulin resistance which intially is matched by B-cell compensation (increased insulin secretion from B-cells and NL BG) but over exhaustion leads to B-cell failure (decreased insulin release and overt DM)

31
Q

key features of VIPoma

A

-tumor of D1 cells (increased vasoactive intestinal peptide secretion)
-causes increase in intestinal fluid secretion
sx of WDHA syndrome: watery diarrhea, hypokalemia, achlorhydria (lose K+ and Cl-) , and 20% will experience flushing (like in carcinoid tumor of pancreas)

32
Q

key features of somatostatinoma

A
  • somatostatin functions as a paracrine regulator, so it typically manifests as inhibitory
  • reduced insulin –> DM
  • reduced GB motility–> cholelithiasis
  • reduced exocrine pancreatic secretions–> steatorrhea

**HARD TO DX bc mimics other pathologies

33
Q

What is the MHC HLA gene associated with T1DM

A

HLA DR/DQ gene on Chr 6p21

34
Q

define incretins

A
  • MOA: “assist”/ stimulate insulin release and inhibit glucagon release resulting in a lower BG
  • stimulated by oral glucose in the GI tract
  • inactivated by DPP-4 (dipeptidyl peptidase-4)

Examples: GLP-1 and GIP
(glucagon like peptide 1 and glucose dependent insulin releasing polypeptide)
**GLP activated insulin release and inhibits glucagon **

35
Q

effects of advanced glycated end products (AGE) binding to receptor in the setting of hyperglycemia/DM

A
  1. activation of cell signaling molecules : Protein Kinase C (PKC)!!, MAPK, and NFkB
  2. effects on vasculature/heart:
    - cytokines and growth factors (TGF-B & VEGF)
    - ROS production
    - procoagulant activity (embolism, MI, strokes)
    - proliferation of smooth muscle (cardiomegaly)
    - cross linking of matrix proteins (proatherogenic = CAD)
36
Q

how to tx DKA

A

insulin
hydration
potassium ! (giving insulin puts K+ back into cells therefore pts rapidly lose K+; even though the initial decrease in insulin from DKA causes it to look like hyperkalemia)

37
Q

changes seen in the eye of a patient with diabetic retinopathy

A
  1. neovascularization (growing off distorted vessels that cause hemorrhage and blindness)
    - pathogenesis: hypoxia leads to VEGF over expression
  2. cotton wool patches (retinal infarcts from hypoxia)
  3. narrow arterioles from damage
38
Q

effects of insulin on adipose tissue, striated muscle, and liver

A
  1. adipose
    - increase glucose uptake, increase lipogenesis (anabolic), decrease lipolysis
  2. muscle
    - glucose uptake, glycogen synthesis, protein synthesis
  3. liver
    - decrease gluconeogenesis, increase glycogen synthesis, increase lipogenesis

Hannah Endo/Repro year 2 (11 decks)

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