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Pathophysiology > module 13 DM > Flashcards

module 13 DM Flashcards

1
Q

Type 1

A

autoimmune destruction of Beta cells
type IV hypersensitivity
s/s do not arise until sufficient destruction has occurred, could be years after the initial trigger

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2
Q

type 2

A

insulin resistance

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3
Q

other types of diabetes

A 
maturity onset diabetes of youth 
- genetic defect in insulin production or release
Gestation DM 
- during preg
Various endocrine disorders
- cushings
- acromegaly
- pheochromocytoma
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4
Q

Type 1 clinical

A 
onset < 20
normal weight
dec. blood insulin 
anti-islet cell antibodies 
ketoacidosis is common
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5
Q

type 2 clinical

A

obese
inc. blood insulin
no antibodies
HHNK more common

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6
Q

Type 1 DM: 2 forms

A 
1A: immune mediated 
- 3 subcategrories 
-- polygenic
-- monogenic
-- latent autoimmue 
1B: idiopathic
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7
Q

polygenic 1A

A

2 or more genetic loci

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8
Q

monogenic 1A

A

rare assoc with IPEX syndrome

  • immune dysfunction
  • polyendocinopathy
  • enteropathy
  • X-linked
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9
Q

latent autoimmune 1A

A

development of T-cell reactivity in adulthood

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10
Q

Acute complications of DM

A

hypoglycemia: over tx
diabetic ketoacidosis
- no energy in cell, rely on fatty acid’s to work
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)

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11
Q

ketogenesis

A

ketone bodies: used to generate energy without glucose

  • acetoacetate
  • acetone
  • B-hydroxybutyrate
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12
Q

HHNK vs DKA

A 
Glucose: HHNK(900) > DKA(600)
Na: HHNK: high, DKA: nml
pH: HHNK: slightly low, DKA: very low
Bicarb: HHNK: slightly low, DKA: very low
anion gap: DKA elevated
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13
Q

Risk factors DM type 2

A

aging
sedentary lifestyle
obesity
- inc. abd. fat inc. risk

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14
Q

chronic complications of DM

A 
hyperglycemia and nonenzymatic glycosylation 
microvascular disease
- retinopathy
- nephropathy
- cardiomyopathy
Macrovascular disease
- coronary artery disease
- stroke
- peripheral arterial disease
- accelerated atherosclerosis 
diabetic neuropathy
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15
Q

glycosylation

A

glycosylation end products (AGE’s)

  • proteins that bind to glucose
    inc. glucose -> inc. binding -> inflammation
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16
Q

AGE chemical properties

A 
cross link polypeptides of same protein
trap nonglycosylated proteins (LDL) 
confer resistance to proteolytic digestion 
induce lipid oxidation 
inactivate nitric oxide
bind nucleic acids
17
Q

AGE bind to receptors and induce

A 
monocyte emigration 
cytokine and GF secretion 
inc. vascular permeability
procoagulant activity
enhanced cellular prolieferation 
enhanced ECM production 
proinflammatory
18
Q

AGE/glycosylation adverse effects

A 
microangiopathy, cerebravascular infarcts 
HTN
retinopathy, cataracts, glaucoma
MI
gastoparesis
Islet cell loss 
Atherosclerosis
peripheral vascular disease
-> infections, gangreen 
peripheral neuropathy 
nephroscerolsis
- glomerulosclerosis
- arteriosclerosis
- pyelonephritis
19
Q

retinopathy

A

background diabetic retinopathy: earliest phase
- arteriesi n retina become weakened and leak, forming small, dot-like hemorrhages
Proliferative retinopathy: later stage
- circulation problems cause ischemia -> neovascularization that leak

20
Q

nephropathy

A

hyperglycemia-> inc. renal blood flow
-> inc. glomerular capillary pressure -> inc. protein excretion -> glomerular damage -> dec. GFR and renal failure, and HTN

21
Q

glomerular damage DM

A

protein excretion -> glomerular damage

  • loss of negative charge
  • glomerulosclerosis
  • thickening of basement membrane
  • mesangial expansion
22
Q

neuropathy

A

peripheral neuropathy causes either pain or loss of feeling in toes, feet, legs, hands, and arms
- pressure injury will go unnoticed
glucose-> neuron: H2O follows -> swelling and inflammation

23
Q

Autonomic neuropathy

A

causes changes in digestion, bowel and bladder function, secual response, and perspiration

24
Q

focal neuropathy

A

results in sudden weakness of one nerve, or a group of nerves -> weakness or pain

25
Q

Type 2 prevention

A

exercise: muscle uptake of glucose independent of insulin
diet: losing weight increases insulin sensitivity

26
Q

Prediabetes

A

fasting plasma glucose 100-125
GTT: 140-199
HbA1C: 5.7-6.4

27
Q

diabetes dx

A 
fasting plasma glucose: > 126
OR
s/s of hyperglycemia and casual glucose > 200 
GGT: >200 
HbA1C: > 6.5
28
Q

hyperglycemia classic s/s

A

polyuria
polydipsia
unexplained wt loss

29
Q

Dawn phenomenon

A

liver released glucose in morning for energy to start day

- body has no insulin -> inc. glucose

30
Q

Symogyi effect

A

inc. BG in mornind d/t insulin injection before bed
not enough -> inc. glucose
too much -> liver responds to dec. glucose by giving more

Pathophysiology (80 decks)

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