PANCREAS- DM COMPLICATIONS, DISORDERS OF METABOLISM Flashcards

1
Q

macro v. microvasc complications

A

macro
- CAD, PAD, CVA/stroke

micro
- diabetic nephropathy, retinopathy, neuropathy

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2
Q

macrovascular complications

A

DM causes accelerated athersclerosis of vessels and inc risks of :

CAD- inc risk MI, CHF
- MI is MCC of death in DM

PAD- can lead to limb ischemia
- risks of gangrene in the feet inc

CVA/stroke

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3
Q

macrovascular complications pathophys

A

atherosclerosis
- cholesterol, fibrin, calcium, and cellular waste builds up and sticks to artery walls
- build up causes narrowing and stiffness
- restrict bf, causes turbulent flow, harder for RBC to reach vessel walls and deliver oxygen

organs can be starved of oxygen, leading to MI, strokes, and ischemia

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4
Q

macrovascular complications- tx and goals

A

REDUCE RISK FACTORS
- smoking cessation, diet, exercise

  • strict glycemic control (A1C<7%)
  • aggressive BP and lipid control
    —->goal SBP <130, ramipril dec MI, CVA, CVD death
    —–> goal LDL <70, statins
  • +/- daily low dose ASA if high CV risk and not CI
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5
Q

microvasc complications affect:

A
  • damage to small blood vessels leading to atherosclerosis of arterioles
  • thickening of capillary basement membrane (dec oxygen to surrounding tissues and nerves)
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6
Q

microvasc complications

cause of diabetic nephropathy
- higher risk in what type of DM?

A

due to glomerular sclerosis or basement membrane thickening
- leading cause of ESRD
- 30-40% risk within 20 yrs of dx DM1 (less risk w DM2)

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7
Q

microvasc complications

diabetic nephropathy
- screening for?
- dx for DM1 vs. 2
- untreated dx

A

+ microalbuminuria
- damaged glomeruli cause protein leak into urine

dx: urine albumin/creatinine ratio (ACR) >=30
- DM1: check 5 yrs after dx and then Q1yr
- DM2: check at onset, then Q1yr

untreated: progresses to overt proteinuria
- ACR >= 300/24hr
- exacerbates and worsened by HTN
- decreases GFR –CKD—progress to ESRD

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8
Q

microvasc complications

diabetic nephropathy
- tx

A
  • control glucose (A1C<7%), BP (SBP <130), lipids (LDL<70), and lifestyle mods
  • ALL DM pts w + ACR start on ACE/ARB for renal protection
  • DM2 + ACR and GFR >20—> consider adding SGLT2i (-flozin)

SGLT2i better for CKD

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9
Q

microvasc complications

diabetic retinopathy types

A

nonproliferative- most cases
- weakening of retinal vessels leads to aneurysms, bleeding, dilation, retinal swelling

proliferative- neovascularization (new vessels in retina) and scarring

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10
Q

microvasc complications

non proliferative retinopathy
- clinical presentaiton
- fundoscopic exam

A

asymp presentation unless edema or ischemia of retina involves macula
- MCC vision loss in DM pts –> MACULAR EDEMA

fundoscopic exam- hemorrhages, cotton wool spots, exudates, microaneurysms, venous dilation

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11
Q

microvasc complications

proliferative retinopathy
- clinical presentation
- fundoscopic exam

A

neovascularization

fundoscopic exam: watch for vitreous hemorrhage and retinal detachment (urgent eval)
- can lead to blindness, requires immediate laser eye surgery

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12
Q

microvasc complications

retinopathy screening and management (which tx for prolif/mac edema)

A

screening
- annual w ophthalmologist, dilated eye exam

management
- gluc, BP, lipid control to prevent/stop progression

PROLIFERATIVE TX
- laser photocoagulation to shrink.destroy abnorm retinal structures/vessels

PROLIF and MACULAR EDEMA w VISION LOSS
- intravitreal injx of anti-VEGF to stop/dec growth new BV and fluid buildup
—-> ranibizumab, brolucizumab

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13
Q

microvasc complications

diabetic neuropathy
- types and their subtypes

A

MC complication, due to restriction BF to nerves
- diffuse neuropathy: peripheral or autonomic
- mononeuropathy: isolated nerves (cranial or peripheral) or mononeuritis multiplex
- radiculopathy: diabetic amyotropy or thoracic radiculopathy

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14
Q

diffuse neuropathy: peripheral (MC)
- presentation
- test

A
  • numbness & paresthesia in B/L stocking glove pattern
  • causes ischemia in areas of pressure–>ulcer–>infection
  • first dec vibration, second dec pinprick sensation on monofilament test (PE), lastly dec in general sensation
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15
Q

diffuse neuropathy: peripheral
- painful neuropathy and its tx

A

SEVERE burning and hypersensitivity most notable at night
- tx: pregabalin, TCA (nortriptyline, amitryptiline), gabapentin

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16
Q

diffuse neuropathy: peripheral
- complications

A
  • charcot foot—>osteomyelitis–>amputation
  • diabetic foot
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17
Q

diffuse neuropathy: peripheral
- diabetic foot complications and management

A

DIABETIC FOOT
- ulcer and infections that lead to amputation if not treated (very difficult to treat once reaches bone)

management
- tx bruises, cuts, ulcers
- advise pt to inspect feet DAILY and see podiatrist yearly
- therapeutic footwear

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18
Q

diffuse neuropathy: peripheral
- charcot foot complication

A

inability to sense/feel injuries and accomodate wt
- can cause bone, destruction subluxation, dislocation, deformity
- Rocker bottom foot (deformity)

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19
Q

diffuse neuropathy: autonomic
- presentation
- MC presenations

A
  • can affect any single organ or multiple, diagnosis of exclusion

MC
- impotence!
- gastroparesis!
- orthostasis
- neurogenic bladder
- enteropathy

20
Q

diffuse neuropathy: autonomic
- prevention
- pharm tx

A

prevent ds progression
- modifiable RF (HLD, HTN, smoking, GLC control)

pharm tx individual to each condition
- sildenafil for impotence
- prokinetic agents, antiemetic in gasoparesis (metoclopramide)
- high salt, fludrocortisone or midodrine for orthostat hypotension

21
Q

mononeuropathy: isolated cranial mononeuropathy
- what nerves affected
- presentation, functions affected

A

CN III (oculomotor MC), IV (trochlear), and or VI (abducens)
CN VII

presentation (II, IV, VI)
- unilat eye pain and external deviation
- ptosis and diplopia
- PUPILLARY FUNC REMAINS INTACT

CN VII- bells palsy
- unilat facial paralysis (cannot wrinkle brow, dropping eye lid, cant puff cheek, droop corner of mouth)

ptosis- droopy eyelid

22
Q

mononeuropathy: isolated peripheral nerve damage
- nerves damage and affected functions

A
  • median or ulnar (MC): numb, tingling, weakness in hand/arm
  • peroneal mononeuro: sciatic nerve branch, foot drop
  • thoracic neuro: numb/tingling or pain along intercostal dermatome
23
Q

radiculopathy or polyradiculopathy: diabetic amyotrophy
- nerves affected
- presentation

A

MC type of DM polyradiculopathy

nerves
- lumbosacral nerve roots and periph nerves

presentation
- acute, assym, pain followed by weakness involving proximal leg, w quads wasting and wt loss
- progression over months followed by partial recovery, recurrence in most pts

24
Q

radiculopathy or polyradiculopathy: thoracic
- nerves affected
- presentation

A
  • multiple thoracic nerve roots
  • severe thoracic or abd pain, band like pattern
25
DM monitoring and screening for complications - list all
- PCP visits, A1C, FSG (AC/HS), BP, lipid panel, yearly podiatry, ophtho, spot microalbumin (ACR), BMP, prevnar 20 after 19 yo (pneumococcal vax)
26
DM complications screening goals - PCP - A1C - FSG - BP - lipid panel - ophtho
- PCP: 2-4x a year (A1C, foot check, BP check) - A1C: check at dx then q3m until controlled, then q6m>>12m (goal <7%) - FSG (AC/HS): rx glucometer, goal 80-130 fasting, <180 peak postprandial - BP: SBP goal <130/80, add ACE/ARB in DM w early nephropathy or HTN - lipid panel: statin in DM if LDL>70 - yearly podiatry - ophtho: dilated exam - spot microalbumin ACR - prevnar 20 after 19 yo
27
Diabetic ketoacidosis (DKA) - which pts - patho
DM1 pts patho: - body perceived in starvation state causes break down of free fatty acids - FFA converted into ketone bodies which accum hydrogen ions in blood causing dec in pH of blood---> ACIDOSIS
28
DKA factors (causes)
- inadequate insulin administration - stress (illness, infx, trauma, surgery, stroke, MI, bleeding, dehydration)
29
DKA presentation and onset
RAPID ONSET - kussmaul respirations: deep labored rapid breaths - sweet fruity breath - n/v abd pain - mental status changes (lethargy-->coma) - polydipsia, polyuria, polyphagia (3 P's)
30
DKA Dx
triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia - serum GLC >250 - metabolic acidosis (pH <7.3) w elevated anion gap >12 - (+) ketones (acetone or B-hydroxybutyrate)
31
DKA- what other labs might pts present with
- often present w hyperkalemia and hyponatremia hyperkalemia: ****** numbers appear high (K is exracellular) but overall K+ stores in body are low and often need repletion during Tx hyponatremia: pseudohyponat - osmotic shift ICF to ECF, appears low
32
DKA management
admitted to ICU - NPO - IV fluids immed - IV vs SC INSULIN infusion- start after IV fluid and confirm K+>3.5 - potassium repletion (goal K+ 4-5) - bicarb if pH<7 - cultures/CXR for possible infx source - check FSG q1h and BMP (AG, electrolytes, Cr) q2-4 for med adjustments
33
Hyperosmolar hyperglycemic state (HHS) - what pts
high plasma osmo due to hyperglycemia, severe dehydration, +/- obtundation (reduced alertness), but WITHOUT acidosis - higher risk mortality compared to DKA - DM2 pts
34
HHS - patho
- severe hyperglycemia causes osmotic diuresis leading to profound dehydration - ketosis and subseq acidosis is minimal/absent (gluc levels 1000 before sx begin)
35
HHS - presentation - onset
SLOWER onset, also precipitated by stress state presentation - polydipsia - polyuria - signs of extreme dehydration (hypotensive/tachycardia) - neuro findings: MS CHANGES more common (lethargy-->confusion-->seizures--->coma)
36
HHS - dx
- admission pH > 7.3 - serum bicarb >18 - hyperglycemia (>900) - serum osmo >320 - neg for ketones in serum and urine
37
HHS - management
almsot same as DKA with more aggressive initial IVF - NPO - IVF START IMMED - IV insulin infusion (check K+ ensures >3.5 and replete as needed to maintain 4-5) - check FSG q1h, BMP q2-4h, PanCx look for source
38
hypoglycemia - cause, which organ at highest risk - what gluc levels show sx
due to imbalance of insulin and glucagon - hypoglycemia outside of pts with treated DM is uncommon - BRAIN most at risk - gluc approach 80 production dec insulin production, approach 50 pt is symptomatic
39
hypoglycemia - causes - symptoms
causes - exogenous insulin (MCC), insulinoma, meds (sulfonylureas), liver failure, adrenal insuff symptoms - start at Glc = 50 - neuroglycopenia: irritability, behavioral change, weak, drowsy, HA, confusion, convulsions, coma, death - inc epinephrine: sweating, tremor, HTN, anxiety and palpitations
40
hypoglycemia - dx
check FSG (Sx start glc 50) - LOOK FOR UNDERLYING CAUSE - pt on insulin (MCC)--> pt shows inc insulin levels and dec C peptide (exogenous does not contain C pep) - pt taking sulfonylurea: ask in Hx, check drug levels - remainder determined by investigation/hx/presentation
41
hypoglycemia - tx (FSG 54-70, <54, initial tx monitoring)
FSG 54-70 and able to tolerate PO (awake) - 15-20 g PO glucose (tablets, juice, soda, hard candy, crackers) FSG <54 or cannot take PO - IV dextrose (D50 IV push) (confirm IV access good otherwise can lead to extravasation/necrosis) - no IV access--> glucagon 3 mg intranasally OR 0.5-1 mg SC or IM monitor initial tx - response to IV dextrose and glucagon is transient - need to follow by glkucose infusion or continued PO intake
42
insulinoma - define - symptoms
insulin producing tumor in B cells - assoc w MEN I syndrome (endocrine tumors) symptoms - hypoglycemia <50, associated sx - relief with glucose
43
insulinoma - dx - tx
screen by checking for whipple triad - gluc <50 - neuroglycopenic symptoms - prompt sx relief w glucose - DEC 24-72 hr fasting insulin, INC c peptide tx - surgical tumor resection, diazoxide if inoperable
44
obesity
BMI>=30 - chronic mismatch caloric intake v. expenditure - genetic traits, enviro behaviors - drug induced (steroid, antipsych, antidepress, DM meds, antiepileptics) - endocrine ds: cushings, PCOS
45
obesity screening and management
screen - BMI q1y, waist cirumfrence if BMI >=25 - >40 in men, 35 in women management - initial: diet, exercise, behav mod (<100k/cal, >30 min activity) - pharm: GLP1, orlistat, phentermine - surgical: bariatric tx BMI>40 and failed other options
46
metabolic syndrome
3 or more - abd obesity - high TG - HTN - hyperglycemia - low HDL