A.5 Diabetes Complications. TX DM Flashcards

Question

A.5 Diabetes Complications. TX DM DKA pathophys - Osmotic diuresis and hypovolemia

Answer 1

Insulin normally elevates cellular uptake of glucose from the blood. In the insulin-deficient state of DKA, hyperglycemia occurs. Hyperglycemia, in turn, leads to progressive volume depletion via osmotic diuresis. Insulin deficiency → hyperglycemia → hyperosmolality → osmotic diuresis and loss of electrolytes → hypovolemia

Answer 2

Insulin deficiency increases fat breakdown (lipolysis) through increased activity of hormone-sensitive lipase. Metabolic acidosis develops as the free fatty acids generated by lipolysis become ketones, two of which are acidic (acetoacetic acid and beta-hydroxybutyric acid). Serum bicarbonate is consumed as a buffer for the acidic ketones. Metabolic acidosis with an elevated anion gap is therefore characteristic of DKA. Insulin deficiency → ↑ lipolysis → ↑ free fatty acids → hepatic ketone production (ketogenesis) → ketosis → bicarbonate consumption (as a buffer) → anion gap metabolic acidosis

Answer 3

As a result of hyperglycemic hyperosmolality, potassium shifts along with water from inside cells to the extracellular space and is lost in the urine. Insulin normally promotes cellular potassium uptake but is absent in DKA, compounding the problem. A total body potassium deficit develops in the body, although serum potassium may be normal or even paradoxically elevated. Insulin deficiency → hyperosmolality → K+ shift out of cells + lack of insulin to promote K+ uptake → intracellular K+depleted → total body K+ deficit despite normal or even elevated serum

Answer 4

There is a total body potassium deficit in DKA. This becomes important during treatment, when insulin replacement leads to rapid potassium uptake by depleted cells and patients may require potassium replacement.

Answer 5

BMP: glucose < 33.3 mmol/L Bicarbonate < 18 mmol/L Elevated anion gap > 10 mmol/L Urinanalysis: Moderate-large urine ketones (ketonuria) Glucosuria pH: pH ≤ 7.30 - metabolic acidosis Electrolytes: Hyponatremia - Due to hyperglycemia-induced osmotic shift of intracellular water into the extracellular space. Potassium in DKA: normal or elevated (despite a total body deficit) Magnesium levels are typically low. Phosphorus levels may be elevated despite a total body deficit. BUN and creatinine are often elevated - ↑ BUN and creatinine suggest AKI, which in hyperglycemic crisis is often due to osmotic diuresis and dehydration and typically responds to fluid resuscitation. Persistently elevated BUN and creatinine despite fluid resuscitation should prompt further investigation.

Answer 6

Rapid onset (< 24 h) Abdominal Pain - The state of ketoacidosis leads to irritation of the peritoneum. This can cause diffuse abdominal tenderness on palpation with guarding, possibly even to the extent that an acute abdominal pathology is suspected. Fruity odor on the breath (from exhaled acetone) Hyperventilation: long, deep breaths (Kussmaul respirations) - Respiratory compensation for the state of metabolic acidosis

Answer 7

Initial steps ABCDE approach Urgent diagnostics, e.g., POC glucose, BMP, blood gas analysis Volume status assessment Principal interventions Fluid resuscitation: initially with isotonic saline (0.9% NaCl) Potassium repletion: for potassium level < 5.3 mEq/L Insulin therapy: initiate short-acting insulin once potassium level is > 3.3 mEq/L IV sodium bicarbonate: only for severe refractory metabolic acidosis Identify and treat precipitating causes (e.g., sepsis). Consider endocrine consult and admission to the ICU.

Answer 8

First hour: isotonic saline solution (0.9% sodium chloride) at 15–20 mL/kg/hour (∼ 1000–1500 mL bolus) Next 24–48 hours: Adjust IV fluid rate and composition according to CVP, urine output, blood glucose, and corrected sodium levels. Check corrected sodium for hyperglycemia. If corrected serum sodium ≥ 135 mmol/L: 0.45% NaCl If corrected serum sodium < 135 mmol/L: 0.9% NaCl Switch to a solution containing dextrose (e.g., D5NS) when glucose falls to ∼ 200 mg/dL (DKA) or 300 mg/dL (HHS).

Answer 9

Primarily affects patients with type 2 diabetes The pathophysiology of HHS is similar to that of DKA. However, in HHS, there are still small amounts of insulin being secreted by the pancreas, and this is sufficient to prevent DKA by suppressing lipolysis and, in turn, ketogenesis. HHS is characterized by symptoms of marked dehydration (and loss of electrolytes) due to the predominating hyperglycemia and osmotic diuresis. Relative insulin deficiency (enough to suppress ketogenesis but not enough to prevent hyperglycemia) → Marked hyperglycemia → osmotic diuresis → Profound dehydration → ↑ Plasma osmolality → altered mental status Minimal or no ketosis (due to residual insulin activity)

Answer 10

Polyuria Polydipsia Recent weight loss Nausea and vomiting Signs of significant dehydration Neurological abnormalities Altered mental status Lethargy Coma Other neurological examination abnormalities, e.g., blurred vision and weakness INSIDIOUS/ gradual onset (days) In HHS, residual insulin production prevents significant ketoacidosis leading to insidious progression (days to weeks) and profound hypovolemia and hyperglycemia (> 600 mg/dL).

Answer 11

HHS is the diagnosis in patients with type 2 diabetes who have hyperglycemia and hyperosmolality! HHS: hyperglycemia, hyperosmolality, and dehydration without ketonuria Check serum glucose to confirm hyperglycemia. Check BMP for serum bicarbonate, anion gap, electrolytes, and renal function. Check for the presence of ketones. Urine ketones: Standard urine dipstick assays detect acetoacetate and acetone but not beta-hydroxybutyrate. Serum beta-hydroxybutyrate Check blood gas analysis for pH. Diagnostic workup to evaluate the underlying cause: HbA1c, CBC, ECG, infectious workup

Answer 12

BMP: glucose > 33.3 mmol/L Bicarbonate: > 18 mmol/L Normal anion gap < 10 mmol/L serum osmolarity - Elevated > 320 mmol/kg same tx as DKA

Answer 13

Yes — called euglycemic DKA, often seen with SGLT2 inhibitors, pregnancy, or prolonged fasting.

Answer 14

Pseudohyponatremia from hyperglycemia → use corrected sodium: Corrected Na+ = measured Na+ + 1.6 for every 100mg/dL glucose > 100

Answer 15

It can cause paradoxical CNS acidosis, hypokalemia, and worsened tissue hypoxia.

Answer 16

Cerebral edema (rare in adults, more in children) - Rapid correction of hyperglycemia or osmolality → Fluid shifts into brain cells → cytotoxic edema Low serum sodium or excess hypotonic fluids can worsen it Seizures Thromboembolism (hyperviscosity) Rhabdomyolysis Acute kidney injury

Answer 17

Start fluids before insulin — dehydration is more severe than in DKA Avoid rapid correction → risk of cerebral edema No ketosis = HHS (think "sweet but not sour") Use corrected Na⁺ to guide fluid choice: use corrected sodium: Corrected Na+ = measured Na+ + 1.6 for every 100mg/dL glucose > 100

Answer 18

Severe hyperglycemia (>600 mg/dL) Hyperosmolarity (>320 mOsm/kg) Minimal or no ketones/acidosis

Answer 19

Because patients still have enough residual insulin to suppress ketogenesis, but not enough to control hyperglycemia

Answer 20

When glucose drops to <300 mg/dL, to prevent hypoglycemia and allow continued insulin infusion to close the osmotic gap

Answer 21

vascular disease of the retina that is usually asymptomatic in the early stages but can lead to visual impairment and blindness as the disease progresses.

Answer 22

Nonproliferative diabetic retinopathy (NPDR) Proliferative diabetic retinopathy (PDR) Diabetic macular edema (DME)

Answer 23

Retinal vessel microangiopathy → blood leaks → retinal hemorrhages Microaneurysms Caliber changes in veins Intraretinal hemorrhage Hard exudates Retinal edema Cotton-wool spots Intraretinal microvascular abnormalities (IRMA)

Answer 24

Mild NPDR to moderate NPDR: Observation only; repeat dilated comprehensive eye examination every 6–12 months. Severe NPDR: Treat as proliferative retinopathy with panretinal laser photocoagulation (PRP) and/or anti-VEGF therapy.

Answer 25

Retinal vessel microangiopathy → chronic retinal hypoxia → abnormal proliferation of blood vessels → traction on retina → retinal detachment Findings of nonproliferative retinopathy are usually present. Neovascularization is the hallmark of PDR Fibrovascular proliferation → vitreous hemorrhage, traction retinal detachment Rubeosis iridis → secondary glaucoma

Answer 26

Proliferative retinopathy: PRP and/or anti-VEGF therapy Both PRP and anti-VEGF therapy are equally effective. PRP is usually preferred as treatment occurs in a single session (reduces risk of loss to follow-up). Anti-VEGF injections alone can be considered for patients who are highly motivated and have no barriers to follow-up.

Answer 27

Retinal vessel microangiopathy → blood leaks → retinal hemorrhages → retinal infiltration with lipids and fluid → macular edema Clinically significant retinal thickening and edema involving the macula, associated hard exudates May occur in all stages of NPDR and PDR

Answer 28

Center-involving macular edema First line: Intravitreal anti-VEGF therapy Consider PRP or focal and/or grid laser depending on severity of retinopathy. Noncenter-involving macular edema: PRP, anti-VEGF, or focal and/or grid laser therapy may be used depending on severity of retinopathy. Refractory disease or severe complications (e.g., tractional retinal detachment, vitreal hemorrhage): Consider vitrectomy.

Answer 29

DR is a microvascular complication — like nephropathy and neuropathy VEGF = key mediator of neovascularization → target of anti-VEGF therapy Macular edema = most common cause of vision loss in diabetics PDR = most dangerous stage → can cause blindness

Answer 30

Inhibits VEGF → reduces neovascularization and vascular leakage → treats DME and PDR

Answer 31

Optical Coherence Tomography (OCT)

Answer 32

Hyperglycemia → endothelial damage, pericyte loss → capillary leakage and ischemia → VEGF release → neovascularization → hemorrhage and fibrosis.

Answer 33

A form of chronic kidney disease that occurs in 20–40% of patients with diabetes mellitus. Caused by glomerular damage induced by glycosylation of the basement membrane and plasma hyperfiltration.

Answer 34

Risk factors Hypertension and blood pressure variability Longstanding diabetes Inadequate glycemic control

Answer 35

Chronic hyperglycemia → glycation (also called non-enzymatic glycosylation or NEG) of the basement membrane (protein glycation) → increased permeability and thickening of the basement membrane and stiffening of the efferent arteriole → hyperfiltration (increase in GFR) → increase in intraglomerular pressure → progressive glomerular hypertrophy, increase in renal size, and glomerular scarring (glomerulosclerosis) → worsening of filtration capacity

Answer 36

Mesangial expansion Glomerular basement membrane thickening Glomerulosclerosis (later stages) Diffuse hyalinization (most common) or Pathognomonic nodular glomerulosclerosis (Kimmelstiel-Wilson nodules): Glomerular capillary hypertension and hyperfiltration → increase in mesangial matrix → eosinophilic hyaline material in the area of glomerular capillary loops Can progressively consume the entire glomerulus → hypofiltration (↓ GFR)

Answer 37

Patients are usually asymptomatic in the early stages; some may report foamy urine. Late Stage hypertension volume overload

Answer 38

Urine Albumin-Creatinine Ratio (ACR) First morning spot urine test 30 mg/g = abnormal Screening for diabetic kidney disease Onset T1DM: 5 years after diagnosis T2DM: from the time of diagnosis Recommended assessment eGFR ≥ 60 mL/min/1.73 m2: Check urine albumin levels and eGFR once a year. eGFR < 60 mL/min/1.73 m2: more frequent assessment is required; see Diabetic kidney disease is confirmed through: Laboratory studies showing persistent (≥ 3 months) albuminuria and/or reduced eGFR

Answer 39

Glycemic targets Measure HbA1c at least twice yearly. An HbA1c of < 6.5–8% is generally recommended. HbA1c may not be an accurate method of glucose monitoring in patients with an eGFR < 30 mL/min/1.73 m2; consider continuous glucose monitoring. Pharmacotherapy T1DM: Insulin dosage may need to be reduced as eGFR declines T2DM Choice of treatment depends on eGFR; eGFR ≥ 30 mL/min/1.73 m2 First line: metformin AND/OR an SGLT-2 inhibitor Consider GLP-1 receptor agonist for patients: Unable to take first-line medications eGFR < 30 mL/min/1.73 m Discontinue metformin. SGLT2 inhibitors can be continued but should not be initiated in patients with eGFR < 20 mL/min/1.73 m2. Selected dipeptidyl peptidase 4 inhibitors, GLP-1 receptor agonists, insulin, thiazolidinediones, and short-acting sulfonylureas can be use

Answer 40

Microalbuminuria (30–300 mg/day)

Answer 41

SGLT2 inhibitors (e.g., empagliflozin) and GLP-1 RAs (e.g., liraglutide)

Answer 42

❌ No — diagnosis begins with microalbuminuria

Answer 43

✅ Only if creatinine rises >30% from baseline or potassium >5.5 → otherwise, continue and monitor

Answer 44

progressive nerve injury caused by chronic hyperglycemia. Distal symmetric polyneuropathy and autonomic neuropathy are the most common types; less common manifestations include mononeuropathy and radiculopathy. Patients with distal symmetric polyneuropathy typically present with sensory loss of the lower extremities and may also have motor weakness, although many affected individuals are asymptomatic.

Answer 45

Diabetic polyneuropathy is the most common form of polyneuropathy in high-income countries. [2][3] ∼ 50% of patients with diabetes develop peripheral neuropathy. [4] Up to 90% of patients with diabetes may develop autonomic neuropathy.

Answer 46

Chronic hyperglycemia causes glycation of axon proteins and subsequent development of progressive sensomotor neuropathy; typically affects multiple peripheral nerves. Chronic hyperglycemia leads to: Sorbitol accumulation in nerves via aldose reductase Oxidative stress Ischemia from microvascular damage (vasa nervorum) → Axonal degeneration + demyelination

Answer 47

Most common type — "glove and stocking" sensory loss Affects distal limbs bilaterally Symptoms: Numbness Tingling Burning pain (worse at night) ↓ vibration, proprioception Loss of ankle reflexes ↑ risk of foot ulcers, Charcot joints

Answer 48

Autonomic Neuropathy Involves involuntary functions CV Resting tachycardia, orthostatic hypotension GI Gastroparesis, diarrhea, constipation GU Erectile dysfunction, neurogenic bladder Sweat Anhidrosis or excessive sweating

Answer 49

Cranial (CN III palsy) - Ptosis, diplopia with pupil sparing Truncal mononeuropathy - Thoracoabdominal pain or paresthesia Limb mononeuropathy - Entrapment syndromes (e.g., carpal tunnel) Diabetic amyotrophy - Painful asymmetric thigh weakness, weight loss (elderly men), self-limiting

Answer 50

TCAs Amitriptyline (watch for side effects in elderly) SNRIs Duloxetine Gabapentinoids Gabapentin, pregabalin Topical Capsaicin cream, lidocaine patches

Answer 51

Gastroparesis: Small meals, metoclopramide or erythromycin Orthostatic hypotension: Fludrocortisone, midodrine Erectile dysfunction: PDE-5 inhibitors (e.g., sildenafil) Neurogenic bladder: Intermittent catheterization, alpha-blockers

Answer 52

✅ This is a classic sign of autonomic neuropathy with compensatory hyperhidrosis in areas where innervation is preserved.

Answer 53

✅ Yes — due to autonomic dysfunction of the GI tract, leading to erratic motility.

Answer 54

Prevalence: more common in patients with type 2 diabetes Risk factors: The major determinants are metabolic risk factors, which include obesity, dyslipidemia, and arterial hypertension. Hyperglycemia may be less related to the development of macrovascular disease. Manifestations Coronary heart disease (most common cause of death) Cerebrovascular disease Peripheral artery disease (possible loss of limb) Monckeberg arteriosclerosis Gangrene

A.5 Diabetes Complications. TX DM Flashcards

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