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diabetes Flashcards

1
Q

what is the number 1 cause of death in diabetic patients

A

cardiovascular - atherosclerosis from chronic inflammation, narrowing of arterial walls myocardial infarction

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2
Q

what type of disease is related to type 2 diabetes

A

hyperlipidemia should be managed low hdl and elevated TG

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3
Q

what are examples of microvasular complications in diabetic patients

A

diabetic nephropathy, retinopathy, neuropathy

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4
Q

macrovascular complications in diabetic patients

A

CAD, Peripheral artery disease, stroke

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5
Q

what does diabetes cause that would affect patients daily life

A

blindness

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6
Q

how many times do u check for diabetic retinopathy

A

screen at diagnosis then annualy

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7
Q

what is the diff for type 1 and 2 diabetes in screening for retinopathy

A

for type 2: screen at diagnosis then annually
for type 1: first screening should be 5 yrs after diagnosis then annually

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8
Q

what do u see in pre- proliferative retinopathy

A

cotton wool spots (infarcts)
venous bleeding
hemorrhages (retinal ischemia)

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9
Q

proliferative retinopathy

A

neovascularization
vitreous hemorrhage

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10
Q

maculopathy

A

suspect if acquity , damage to macula

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11
Q

what is cataract

A

may be juvenile “snowflake form”
early onset “senile “

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12
Q

Rubeosis iridis

A

new vessels on iris occurs late

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13
Q

what are symptoms of peripheral neuropathy that occur in diabetic pts

A

symmetrical numbness, pain , parastesia
absent reflexes and loss of vibratory sense
microfilament testing (annually)

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14
Q

what is responsible for 50% of non traumatic amputations

A

diabetes

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15
Q

what is mononeuropathy

A

affect single nerve or nerve trunk
vascular in origin
sudden foot drop, wrist drop , paralysis CN 3,4,6

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16
Q

autonomic neuropathy symptoms in daibetes

A

orthostatic hypotension and syncope
difficulty swallowing, delayed gastric emptying, constipation, diharrea

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17
Q

what is the first line treatment of type 2 diabetes

A

metformin

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18
Q

what is the MOC of metformin

A

it reduces gluconeogenesis in liver without causing hypoglycemia and increase insulin sesitivity

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19
Q

what are side effects of metformin

A

anorexia and diharrea
lactic acidosis is a srs side effect in pts with renal or liver disease so contraindicated.

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20
Q

what drug can be used inncase of liver or renal failure in diabetic pts

A

sulfonylureas - the 3 Glis
glibenclamide, gliclazide, glipizide

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21
Q

what is the MOC of sulfunylureas

A

works on beta cells to promote insulin secretion

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22
Q

what is the most common side effect of sulfunylurea

A

-prolong hypoglycemia admit to hospital for glucose support
-weight gain - avoid in overweight pts

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23
Q

what group of oral hypoglycemics are cheap and effective in achieving short term (1-3yrs) glucose control

A

sulfunylureas , however effect wears off as b-cell mass declines

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24
Q

what does thiazolidinediones bind to and activate

A

peroxisome proliferator- activated receptor gamma (PPAR-y) a nuclear receptor which regulates genes involved in lipid metabolism and insulin action

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25
side effects of thiazolidine
weight gain, fluid retention, anemia, osteoporosis, bladder cancer
26
what is contraindicated in pts with heart failure
thiazolidinedione
27
what are incretins
group of hormones that regulate blood glucose by enhancing insulin secretion in response to food. mimic GIP and GLP-1
28
GLP-1 and GIP
both secreted by intestine in response to food increase insulin secretion, reduce glucagon secretion, slow gastric emotying
29
what are two main classes of drugs that target incretin system
GLP-1 and DPP-4
30
what is MOC of gliptins (sitagliptin)
inhibiy dipeptidyl peptidase (DPP-4) enzyme which inactivates GLP-1
31
SGLT2 inhibitors (flozins)
reabsorb glucose in kidneys by targeting sglt2 protein in proximal tubule blocking it so more is excreted in urine than absorbed
32
what drug causes genital candidiasis and UTI
SGLT2 inhibitors
33
what is the suggested pathway of tx for type 2 diabetics
monotherapy: metformin if mono not working : metformin + SGLT2 inhibitor triple therapy: metformin, glp1 , sglt2 if triple failed : insulin
34
why do we change insulin injection sites
to prevent lipo atrophy or hypertrophy
35
what are three types of insulins
rapid acting insulin , short acting , longer acting
36
what is rapid acting insulin type
novorapid , insulin lispro , insulin glulisin routinely used in type 1 diabetes faster onset and shorter duration of action
37
what is short acting insulin
actrapid insulin start working within 30-60min and lasts 4-6hrs given 15-30 min before meals
38
what are longer acting insulins
insulins premixed with retarding agents are intermediate(12-24 )or long acting (more than 24)
39
NPH
injected twice a day considered intermediate insulin is not steady and stable during the day hit hardest during 6hrs v srs side effect: hypoglycemia nph supposed to be cloudy
40
lantus - insuline glargine long acting
injected same time each day first long acting one time injection background basal glucose control
41
basaglar - insulin glargine
same as lantus, nbut cheaper precepitates in tissue then released
42
toujeo- insulin glargine
concentrated form of lantus 300units in little amount can have same effect bcs sometimes uncomfortable to inject all at once also lasts longer 30-36 hrs more than lantus
43
levemir- insulin detemir
wears off faster than lantus 16-18hrs split twice a day
44
tresiba - insulim degludec
better than levemir last 42 hrs smooth insulin profile stable steady 40% reduction in hypoglycemia
45
what is basal bolus regimen explain and used for who
used for type 1 diabetis one or 2 subcutaneous injections of long acting or intermediate (basal component) and a bolus injection before each meal for rapid acting
46
what is twice daily insulin regimen
used for type 2 that need basal and bolus and want fewer injections contain mixed rapid and intermediate used twice daily before breakfast and dinner
47
hypoglycemia glucose lvl
less than 3
48
symotoms of hypoglycemia
autonomic: sweating, anxiety, hunger, tremor, palpitations neuro: confusion, drowsiness, visual imapirment personality changes
49
causes of hypoglycemia
errors in tx exogenous drugs P L A I N pituitary insufficiency liver failure addisons disease islet cell tumors non - pancreatic neoplasms
50
true hypoglycemia should be confirmed thru whipples triad
symptoms signs of hypoglycemia low plasma glucose concentration resolution of symptoms after plasma glucose returns to normal
51
what happens to K in hypoglycemia
K gets shifted into cells from insulin so if severe hypoglycemia giving insulin could cause hypokalemia lead to arrythmias
52
where can u see acanthosis nigricans
acromegaly type 2 diabetes cushings
53
what can u check for to know if patient is insulin resistant
check for c-peptide
54
what hormone is usually the most sensitive and only might suspect adenoma if more than 10,000
prolactin
55
what happens to insulin in teenage in dawn
in teens to early adulthood usually GH anatgonizes the effect of insulin so insulin resistant would occur
56
what are secondary management
excercise , lifestyle changes, dash diet, hypertension, lipidemia , overweight
57
incidental adrenal adenoma
usually bilateral is benign
58
what is diabetic ketoacidosis
happens mostly in type 1 diabetes 1) hyperglycemia (>11) usually above 14 in severe 2) ketosis : serum-> B-hydroxybutyric and acetoacetic acid urine-> acetone 3) metabolic acidosis - wide anion gap
59
pathophysiology of diabetic ketoacidosis
1. Insulin Deficiency → Cells cannot use glucose → Hyperglycemia. 2. Increased Lipolysis → Free fatty acids released → Ketone production (β-hydroxybutyrate, acetoacetate). 3. Ketone Accumulation → Metabolic acidosis (high anion gap). 4. Osmotic Diuresis → Dehydration, electrolyte loss (K+, Na+).
60
what happens in diabetic ketoacidosis for resp compensation
kussmaul breathing
61
causes of diabetic ketoacidosis
"5 I's" infection insulin noncompliance infarction (MI+ stroke) intoxication initial diagnosis of type 1
62
what does urine dipstick show in diabetic ketoacidosis
heavy glycosuria ketonuria
63
tx of diabetic ketoacidosis
1L iv saline first hr then 250-500 ml /hr glucose < 14 add 10% dextrose
64
what is resolution of DKA
glucose <11 and 2 of the followimg: bicarbonate <15 PH >7.3 anion gap<12
65
hyperosmolar state diff to diabetic ketoacidosis
affects mainly type 2 no ketones or acidosis (no kussmaul breathimg or fruity breath) no ketones exrtreme hyperglycemia >33.3 ( normal PH, bicarb, anion gap)
66
what causes hyoerosmolar stae
infection and illness prevents breakdown of ketones
67
what do pts with diabetes insipidus presemt with
high vol urine and excess thirst--> vol depletion and hypernatremia hypernatremia= neurological symptoms
68
causes of diabetes insipidus
1. Central Diabetes Insipidus (CDI) – ADH Deficiency • Due to impaired ADH secretion from the hypothalamus or posterior pituitary. 2. Nephrogenic Diabetes Insipidus (NDI) – ADH Resistance • Due to kidney insensitivity to ADH, causing inability to concentrate urine.
69
what is primary polydyspsia (psychogenic)
Not true DI, but excessive water intake suppresses ADH release, causing polyuria. • Causes: • Psychiatric disorders – Schizophrenia, anxiety. • Hypothalamic lesions affecting thirst regulation.
70
diagnosis of DI
The water deprivation test is used to differentiate DI (central vs. nephrogenic) from primary polydipsia. Procedure 1. Stop all fluids for 2-3 hours. 2. Monitor urine output, body weight, and serum osmolality. 3. Give Desmopressin (DDAVP) 2 mcg intranasally or 1 mcg subcutaneously. 4. Check response: - if urine osmolality inc - primary polydypsia - if urine osmal remain low - give desmopressin (vasopressin to diff btwn central and nephro)
71
what is the effect of desmopressin in central and nephrogenic
if urine osmol inc after desmopressin - CENTRAL DI if urin osmol remain low after desmopressin - nephrogenic DI
72
how do u screen for disbetic neohropathy
albumin: protein ratio
73
albumenuria importance in diabtes patient
can lead to diabetic kidney disease then CKD urine albumin to creatinine ratio screening test cant exceed 50%

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