L27- Endocrine Pathology VI (pancreas) Flashcards
list the blood labs that indicate a person is prediabetic
IFG (impaired fasting glycemia): 100-125 mg/dL
IGT (impaired glucose tolerance): 140-199 mg/dL at 2hrs during OGTT
HbA1c: 5.7 - 6.4%
list the acute complications of DM
- hypoglycemia
- diabetic ketoacidosis
- hyperosmolar non-ketotic coma / hyperosmolar hyperglycemic state
- lactic acidosis
DM Acute Hypoglycemia:
- (1) are possible causes
- (2) are clinical features
- (3) is the management
1- missing a meal, excess physical exertion, excess insulin administration
2- dizziness, confusion, sweating, palpitations, tachycardia
3- reversal of hypoglycemia thru oral or IV glucose (prevents onset of neurological damage)
DKA is a more common complication for DM type (I/II). (2) are the possible precipitating factors. Plasma glucose levels will be measured at (3) where this state caused (4) to occur.
1- type I
2- missed insulin, infection / acute illness, trauma, emotional disturbance
3- plasma glucose, 250-600 mg/dL
4- hyperglycemia –> osmotic diuresis and dehydration in DKA
describe the extensive process of DKA
(vicious cycle of progressive metabolic disruption)
- progressive hyperglycemia (precipitating event)
- -> osmotic diuresis / dehydration
- -> cell starvation / hypovolemia
- -> ketosis
i) vomiting via ketosis
ii) electrolyte disturbances via vomiting / osmotic diuresis
iii) metabolic acidosis via ketosis, lactic acidosis
list DKA Sxs
- excess urination
- dehydration / excess thirst
- fatigue, loss of appetite
- vomiting
- hyperventilation (Kussmaul breathing)
- fruity scented breath
- mental confusion
list the lab results that indicate DKA
Urine –> sugar / ketone (+)
Blood: glucose >250 mg/dL, hyperkalemia, hyponatremia
ABG: low pH (<7.3, high anion metabolic acidosis), low bicarbonate
-investigations for precipitating factors
describe DKA management
-saline infusion for fluid loss
Restore metabolic control:
- insulin IV
- K supplements
- Bicarb. (sometimes)
HSS = (1):
- mostly occurs in (2) type patients with DM type (I/II)
- (4) is the main cause
- (5) is the main result, causing (6)
- HSS is managed by (7)
1- hyperosmolar hyperglycemic state (hyperosmolar non-ketotic coma)
2- elderly patients
3- DM type II
4- relative insulin deficiency –> prevents ketosis (can’t prevent hyperglycemia)
5- hyperglycemia, 600-1200 mg/dL
6- dehydration
7- fluid replacement, insulin
describe the general long-term DM complications
Microangiopathic:
- capillaries, arterioles, small BVs
- thickening of BM –> leakiness
- manifests into: nephropathy, retinopathy, neuropathy
Macroangiopathic:
- atherosclerosis (large - medium sized arteries)
- manifests into: IHD, stroke, PVD
(1) is a dangerous complication of DM and is the main cause of ESRF. (2) is the first functional change noted, (3) is the first biochemical sign, and (4) is an important associated screening sign. (1) is prevented in DM by (5).
1- diabetic nephropathy
2- hyperfiltration
3- microalbuminuria (30-300 mg/day)
4- proteinuria (urine albumin >300 mg/day)
5- excellent glucose control + HTN Tx/control
list the lesions of diabetic nephropathy
- Glomerular lesion (1st)
- Renal Vascular lesion / atherosclerosis
- Papillary necrosis / necrotizing papillitis
describe glomerular diabetic nephropathy lesion
1st morphological sign: BM thickening + mesangial expansion
subsequent nodular deposits –> Kimmelstiel-Wilson disease + diffuse glomerulosclerosis
describe renal vascular lesions in diabetic nephropathy
hyaline arteriolosclerosis affecting afferent and efferent arterioles
describe papillary necrosis in diabetic nephropathy
(necrotizing papillitis)
special pattern of acute pylelonephritis
(1) is the most common cause of blindness in people between 30-65 y/o. It present as (2) or (3) form.
1- diabetic retinopathy
2- non-proliferatve retinopathy
3- proliferative retinopathy
list the diabetic ocular complications
- retinopathy
- cataract formation
- glaucoma
list the many features of non-proliferative retinopathy
- intraretinal, preretinal hemorrhages
- Retinal Exudates: soft / microinfarcts OR hard / plasma protein and lipid deposits
- microaneuryms: discrete saccular dilations of retinal choroidal capillaries (small red dots on ophthalmoscope)
- venous dilations (at focal points of weakening via pericyte loss)
- retinal edema (via excess capillary permeability + thickening of retinal capillaries)
list the many features of proliferative retinopathy
- neovascularization and fibrosis
- leads to blindness, especially with macula involvement
- vitreous hemorrhages can result from new capillary formation
- retinal detachment: hemorrhage organization can pull retina off substriatum
describe the presentation of diabetic neuropathy
- paresthesia of the limbs, pain (sensory type)
- muscle atrophy and weakness (motor type)
- impotence, orthostatic hypotenstion, bowel habit changes (autonomic type)
diabetic foot can be caused by….
- ischemia, macroangiopathy
- neuropathy, sensory type
- infection, mainly anaerobic microorganisms
list the general mechanisms of long-term DM complications
- Glycosylation
- Accumulation of polyols in tissues
- free radicals
- HTN, dyslipidemia, obesity, insulin resistance
Glycosylation in DM mainly involves (1) and (2). The products of (2) can progress / metabolize into (3), which has been implicated in (4).
1- BM of capillaries
2- strutural proteins
3- AGE (advanced glycosylation end products)
4- retinopathy (+ other diabetic complications)
describe the general process of accumulating polyols in DM
glucose –> sorbitol –> fructose
- sorbitol accumulation causes osmotic effects + depletion of myoinositol, AAs, K+
- process is involved in mediating neuropathy, cataracts
