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MBBS VI - SpC - Medicine > Endocrine - Diabetes > Flashcards

Endocrine - Diabetes Flashcards

1
Q

Physiology of blood glucose control in fed and fasting state

A

Fed state: High glucose level increases insulin secretion:

  • Utilization of glucose by tissue uptake
  • storage of AA, glucose, FA by ↑hepatic and
    tissue uptake and conversion into storage form

Fasting state: Low glucose level increase glucagon, adrenaline secretion

  • breakdown of tissue stores of glycogen, fat and proteins
  • Increase level of ketone bodies, FA, glucose for use
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2
Q

Physiology of insulin secretion

A

Site: pancreatic islet β cells (core)

Process: high glucose → Increased GLUT-2 uptake into pancreatic cell → glycolysis make ATP → K+ ATP channel activation → depolarization → insulin secretion

Insulin from cleaving of C-peptide from pro-insulin

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3
Q

Causes of DM

A
  1. Type 1: immune-mediated β-cell destruction → absolute insulin insufficiency
  2. Type 2: insulin resistance → relative insulin insufficiency gradually becoming an absolute insulin deficiency
  3. Genetic defects of β-cell dysfunction or insulin action, eg. MODY
  4. Secondary diabetes:
  • Pancreatic diseases (affecting β cells directly): chronic pancreatitis, CA pancreas, pancreatectomy, haemochromatosis
  • Overproduction of hormonal antagonists of insulin (eg. acromegaly, Cushing’s)
  • Drug-induced: glucocorticoids, thyroid hormones, thiazides, α/β-agonists, phenytoin, pentamidine, nicotinic acid…etc
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4
Q

Risk factors of type I DM

A

Genetics
→ HLA-DR and –DQ susceptibility haplotypes (20% if HLA identical)
→ Other genes, eg. proinsulin

Environment: triggering events that cause presentation of β-cell antigen to immune system
→ Viruses, eg. mumps, Coxsackie B
→ Bovine serum albumin (BSA) in cow’s milk in infancy (↑risk of T1DM if on cow’s milk early)
→ Toxins, eg. nitrosamines

Immunological: key in pathogenesis
→ Hygiene hypothesis
→ A/w other autoimmune disorders, (eg. thyroid (2-5%), celiac disease, Addison’s, pernicious anaemia, vitiligo)

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5
Q

Pathogenesis of Type I DM

A

Initiation: environmental triggers cause T-cell-mediated autoimmunity towards pancreatic islet β cells

Onset:

  • Insulitis: lymphocytic infiltrate of pancreatic islets
  • Autoantibodies:
  • Anti-islet cell antibodies, eg. anti-glutamic acid decarboxylase antibody (GAD)
  • Anti-insulin antibody

Result: absolute insulin deficiency

  • Progressive destruction of β-cells → ↓insulin secretion
  • Hyperglycaemia when 80-90% of insulin-secreting ability is loss
  • Hyperglycaemia is toxic to β-cells → further worsen insulin secretion
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6
Q

Clinical presentation of Type I DM

A

Abrupt Onset of Hyperglycaemic symptoms: polydipsia, polyuria, nocturia, fatigue

Rapid weight loss

Complications:

  • Diabetic ketoacidosis
  • Urogenital infections/symptoms, eg. UTI, pruritus vulvae (F), balanitis (M)
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7
Q

Pathophysiology of hyperglycaemic symptoms

A

Hyperglycaemia
→ glycosuria
→ osmotic diuresis
→ polyuria, nocturia
→ dehydration
→ polydipsia, fatigue

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8
Q

Risk factors of Type II DM

A

Genetics: MZ twins concordance rate = 70-90% (higher than T1DM!)
→ Altered regulation of β-cell mass
→ Check first-degree relative with Hx of DM

Obesity: 10× risk for BMI >30

Metabolic syndrome: HTN, hyperlipidaemia, PCOS, NAFLD

Previous conditions: pre-diabetes, gestational DM

Age >45y

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9
Q

Pathogenesis of Type II DM

A

Central obesity:

  • Adipocytes release large amounts of FFA → insulin resistance
  • Adipocytes release adipokines → insulin resistance
  • Low physical activity decrease AMPK activation → ↓glucose uptake + ↓FFA metabolism

Progression:
- Hyperinsulinemic euglycaemia: ↑insulin resistance and insulin secretion
- Impaired glucose tolerance: β-cells cannot handle metabolic load → gradual β-cell failure
Early T2DM: Relative insulin deficiency→ hyperglycaemia and hyperlipidaemia cause toxicity to β-cell
Late T2DM: absolute insulin deficiency

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10
Q

Clinical presentation of Type II DM

A

Commonly asymptomatic at dx

  1. Hyperglycaemic symptoms: fatigue ± polyuria/polydipsia
  2. Weight loss: usually none (insulin level sufficient to suppress lipolysis/glycogenolysis)
  3. Body habitus: obese or non-obese
  4. Complications:
    → Hyperglycaemic hyperosmolar state (HHS)
    → Urogenital infections
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11
Q

Monogeneic forms of DM

Subtypes

A
  1. Permenant neonatal DM (PNDM) - permanent activation of K-ATP channel in Pancreatic B-cell > cannot depolarize and release insulin
  2. Maternally inherited diabetes with deafness (MIDD) - Mutation of mitochondrial genome
  3. MODY2 - Inactivating glucokinase gene mutation > cannot make ATP for depolarization and insulin release
  4. MODY1,3,5 > Transcription factor mutations > cannot express components of TCA cycle, glucose transport, insulin
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12
Q

Maturity onset diabetes of the young (MODY)

  • Presentation
  • Diagnosis
  • Cause
  • Management
A

Presentation: early onset (<25y) non-obese NIDDM patients with -ve islet cell autoAb

Dx: Genetic testing

Cause: various mutations interfering with pancreatic β-cell’s ability to secrete insulin

Inheritance: monogenic AD,

Management: no treatment for MODY2 (long-term outcome similar to healthy), sulphonylureas for MODY1/3

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13
Q

Acute complications of DM

A 
Acute complications:
Diabetic ketoacidosis (DKA) in T1DM

Hyperglycaemic hyperosmolar state (HHS) in T2DM

Stress hyperglycaemia: unmasked by infections, pregnancy, steroid therapy or stroke

Infections eg. urogenital infection

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14
Q

Diagnostic criteria of DM

A

Single measurement of random glucose ≥11.1mmol/L with classic DM symptoms or in hyperglycemic crisis

Two positive tests on different days if asymptomatic
→ Venous plasma glucose-based: Fasting glucose ≥7 mmol/L with ≥8h of fasting; 2h post-prandial glucose ≥11.1 mmol/L in a 75g OGTT
→ HbA1c ≥6.5%

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15
Q

Diagnostic Criteria of pre-diabetes

A

Pre-diabetes: ↑risk of DM and macrovascular Cx but no ↑risk of microvascular Cx

□ Impaired fasting glucose (IFG): fasting glucose 5.6-6.9 mmol/L (6.1-6.9 for WHO)
□ Impaired glucose tolerance (IGT): 2h PPG 7.8-11.0mmol/L after 75g OGTT
□ A1c-based: HbA1c 5.7-6.4%

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16
Q

Outline screening for DM

A

Screening: indicated in BMI ≥23 + more than 1 risk factor

  • First-degree relative with
  • High risk ethnicity
  • History of CVD, HT, HL
  • History of PCOS (female)
  • Physical inactivity
  • Medical conditions with insulin resistance

Yearly test for pre-diabetes

3 yearly test for gestational DM

Yearly testing for normal people over 45, with 3 yearly check-up if normal

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17
Q

Compare type I and II DM

  • Age of onset
  • S/S onset
  • Presentation
A
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18
Q

Compare type I and II DM

  • Significant medical diseases
  • Family history of certain diseases
  • First-line investigations
A
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19
Q

Type II DM does not present with weight loss and DKA

True or False?

How to definitely diff. Type I and II DM?

A

False - Type II DM can progress to absolute insulin insufficiency and present with acute complications

Definitive tests:

  • Auto-Ab: anti-islet cell, anti-GAD (70-80%), anti-insulin (60-75%), anti-IA-2 (65-75%), anti-ZnT8 (70-80%)
  • C-peptide: ↓C-peptide in T1DM, ↑/N C-peptide in T2DM
  • Glucagon stimulation test: inadequate stimulation of insulin secretion in T1DM
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20
Q

Follow-up checks for Type I DM

A
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21
Q

Aims of DM management

A

Patient education

Tx DM with individualized choices

Tx associated coronary risk factors

Regular check for complications

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22
Q

Assessment of glycaemic control

A

HbA1c - 6 monthly if stable, 3 monthly if unstable

Home blood sugar monitoring (HBSM) - Insulin use, before eating, sleeping, exercise

Continuous glucose monitoring (CGM) - nocturnal hypoGly, Postprandial hyperGly, Morning hyperGly

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23
Q

Target HbA1c for DM patients

A
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24
Q

Limitations of HbA1c

Alternative

A

Usually good correlation with average blood glucose except:
→ Variable effect: genetic/chemical alterations of Hb (eg. HbF, HbH (↑), Hbpathies (↓))
→ Falsely High HbA1c: ↑glycation (eg. chronic renal failure), ↓erythropoiesis
→ Falsely Low HbA1c: ↓RBC lifespan (eg. blood loss, haemolysis, hypersplenism), transfusion

Alternative: serum fructosamine (glycosylated serum protein)
→ Use: objective index of overall BG control in the preceding 1-3w
→ Need to correct for serum Alb level if <3.0mmol/L

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25
Q

Treatment outline for Type 1 and II DM

A

T1DM: lifestyle measures + insulin

T2DM:
→ Lifestyle measures alone in early stages (1st line)
→ Lifestyle measures + oral hypoglycaemics if relative insulin insufficiency
→ Lifestyle measures + insulin if absolute insulin insufficiency (advanced)

  • First line: Metformin
  • High risk CVD and CKD > SGLT2 inhibitor or GLP-1
  • No CVD or CKD: DDP-4 inhibitor, SGLT2 inhibitor, TZD, GLP-1RA
  • Need weight loss: SGLT2 inhibitor or GLP-1RA
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26
Q

Dietary management for DM

A

Energy content: 30kcal/kg ideal body weight per day

Composition:
→ 40-50% carbohydrates, 30% fat (<7% saturated/trans fat), 20-30% protein
→ 20-35g/d fibre intake

Other advice:
→ Personalized according to individual preference and culture
→ Consistency of meal timing and quantity
→ Emphasis on ↑fibre food, low-fat dairy products and fresh fish
→ Minimize high energy food, esp those with high glycemic index (GI) and glycemic load (GL)
→ Hypocaloric diet for obese T2DM pt

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27
Q

List all classes of drugs for DM

A
  1. Insulin secretagogues
  2. Incretin mimetics
  3. DDP-4 inhibitors
  4. Insulin sensitizers
  5. a-glucosidase inhibitors
  6. SGLT2 inhibitors
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28
Q

Insulin secretagogues

Examples

MoA

A

Sulfonylureas (SUs)

  • 1G: chlorpropamide, tolbutamide
  • 2G: gliclazide (Diamicron), glibenclamide, glipizide

Meglitinide analogues

  • Repaglinide
  • Nateglinide

MoA

Blocks K+ ATP channel of pancreatic β cells
→ ↑depolarization → ↑insulin secretion

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29
Q

Insulin secretagogues

S/E

Cautions

A

Sulfonylureas:

  • Risk of weight gain
  • High risk Hypoglycaemia
  • C/O poor renal function (high risk hypoGly)
  • No cardiovascular or renal benefits

Meglitinide analogues

  • Risk of weight gain
  • Small risk of Hypoglycaemia
  • No cardiovascular or renal benefits
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30
Q

Incretin mimetics

Examples

MoA

A

GLP-1 analogues

  • Exenatide (weekly)
  • Liraglutide (QD)

Mimics endogenous incretin action → ↑insulin secretion from pancreatic β cells

Slow gastric emptying and weight loss

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31
Q

Incretin mimetics

Benefits, S/E and caution

A

Benefits:

  • Atherosclerotic CVD (dulaglutide, liraglutide)
  • Slow progression of Diabetic nephropathy

S/E:

Pancreatitis

Injection site reaction

Thyroid C-cell tumor

C/O very poor renal function (eGFR < 35)

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32
Q

DPP-4 inhibitors

Examples

MoA

S/E

A

DPP-4 inhibitors

  • Sitagliptin (Januvia)
  • Linagliptin (Trajenta)
  • Vildagliptin (Galvus)

Inhibits DPP-4-mediated breakdown of endogenous incretins → prolong incretin action on β cells

S/E

↑risk of acute pancreatitis and pancreatic CA or neuroendocrine tumours
↑risk of IBD, deranged LFT and rarely joint pain

Caution:

Dose adjustment in CKD (except linagliptin)

Risk of HF (saxagliptin only)

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33
Q

Insulin sensitizers

Examples

MoA

A

Biguanides
- Metformin HCl (Glucophage)

↑AMPK activity → ↓gluconeogenesis, ↑FA utilization, ↓FA synthesis

Thiazolidinediones

  • Rosiglitazone
  • Pioglitazone (Actos)

↑PPARγ action in adipocytes → ↓inflammation, ↑insulin sensitivity,
preferential differentiation of pre-adipocytes to increase FA uptake

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34
Q

Biguanides/ Metformin

Benefits

S/E

Caution

A

Benefits:

  • Weight loss
  • Benefit against ASCVD

S/E

  • GI S/E (dyspepsia, diarrhea) and B12 deficiency

Caution

  • Risk of lactic acidosis: eGFR <30, alcohol abuse, severe liver disease,
    unstable HFrEF or uncontrolled sepsis at risk of hypoperfusion
  • Dose adjustment at eGFR 30-45
  • Withhold 48h before and after contrast CT
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35
Q

Thiazolidinediones

S/E

Caution

A

S/E:

  • weight gain
  • derange LFT
  • Increase LDL-C (Rosiglitazone)
  • Bladder Cancer (Pioglitazone)

Caution:

  • Increase fluid retention and risk of congestive HF
  • C/O Chronic kidney disease
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36
Q

α-glucosidase inhibitors

Examples

MoA

S/E

A

α-glucosidase inhibitors

  • Miglitol
  • Acarbose

Competitive inhibitors of GI α-glucosidase → ↓digestion and absorption of starch and disaccharides from small intestines → ↓postprandial blood glucose level

Lower risk of ASCVD

S/E:

Flatulence and diarrhea due to high glucose in feces

Poor hypoglycaemic effect/ performance

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37
Q

SGLT2 inhibitor

Example

MoA

Benefits

S/E

A

SGLT2 inhibitor

  • Canaglifozin
  • Dapaglifozin (Forxiga)
  • Empaglifozin (Jardiance)

Inhibits SGLT2 in PCT of kidney tubule → ↓glucose reabsorption → ↑glucose excretion

Benefits:

  • Weight loss
  • No hypoglycaemia
  • Reduce ASCVD and Diabetic nephropathy

S/E:

  • Urogenital infections
  • Postural hypotension (osmotic diuresis)
  • Osteoporosis (Canagliflozin)
  • CA bladder (Dapagliflozin)
  • High LDL-C
  • Euglycaemic DKA
38
Q

Insulin therapy

Indication

A

T1DM: Immediately from Dx

T2DM:
→ Features of absolute insulin insufficiency, eg. marked recent weight loss, marked ketosis
→ Failed oral Tx
→ Clinically ill, eg. dehydrated, infection, MI
→ Pregnancy

Features of absolute insulin deficiency: Ketosis, Marked recent weight loss, Underweight/ critically ill

Severe hyperglycemia at Dx: HbA1c >10%, Fasting glucose >16.7mmol/L

39
Q

Forms of insulin

A

□ Rapid-acting analogues, eg. insulin Aspart (Novorapid), insulin Lispro (Humalog)

□ Short-acting insulins, i.e. regular human insulin eg. Actrapid, Humulin R

□ Intermediate-acting analogues, eg. insulin NPH (protaphane)

□ Long-acting analogues, eg. insulin degludec (Tresiba), insulin glargine (Lantus)

□ Pre-mixed insulins, eg. Protamine/Aspart (Novolog 70/30), Lispro protamine/Lispro (Humalog mix 75/25 and 50/50), NPH/regular (Humulin mix 70/30, Novolin mix 70/30)

40
Q

3 types of insulin regimens

2 monitoring methods

A

Basal insulin only: suitable for patients with fasting hyperglycemia only
→ Examples: protaphane bedtime, Tresiba/Lantus OM/bedtime

Daily/BD insulin: suitable for patients with daytime hyperglycemia
→ Examples: protaphane , pre-mixed

Basal-bolus insulin: suitable for patients with difficult titration or T1DM or long term type 2 DM with worsening insulin deficiency
→ Examples: Tresiba + Novorapid

fasting Haemstix for fasting glycemic control

Regular HbA1c for postprandial control

41
Q

4 acute diabetic complications

A

 Diabetic ketoacidosis (DKA) ± coma

 Hyperglycaemic hyperosmolar state (HHS) ± hyperosmolar nonketotic coma (HONK)

 Hypoglycaemia

 Infections: pulmonary TB (due to ↓WBC function), UTI (glycosuria), others

42
Q

Triggers of DKA and HHS

A

Reason: inability to ↑insulin appropriately to compensate for stress hyperglycaemia

Triggers:
→ Physiological stress: infection, operation, trauma, MI, stroke (esp if elderly)
→ Emotional stress if severe
→ Drug administration, eg. steroids

43
Q

DKA

Which type of DM presents with DKA?

Precipitating factors?

Severity levels?

A

Presentation:

  1. Usually T1DM or in advanced, insulin-deficient T2DM
  2. Presenting manifestation of undiagnosed T1DM
  3. Inadequate insulin Tx in known T1DM

Precipitating factors:

  1. Infections (30-40%)
  2. Non-compliance with treatment (25%)
  3. Alterations to insulin dose (13%)
  4. Newly diagnosed DM (10-20%)
  5. MI (<1%)

Severity:

Mild: pH 7.25-7.3, HCO3 15-18, alert
Moderate: pH 7-7.25, HCO3 10-15, mild drowsiness
Severe: pH <7, HCO3 <10, stupor/coma

44
Q

Biochemical profile in DKA

A

□ Ketoacidosis: hyperketonemia and ketonuria with metabolic acidosis
□ Hyperglycaemia: ≥11mmol/L
□ Dehydration and electrolyte disturbances

Mild: pH 7.25-7.3, HCO3 15-18, alert
Moderate: pH 7-7.25, HCO3 10-15, mild drowsiness
Severe: pH <7, HCO3 <10, stupor/coma

45
Q

Pathogenesis of DKA

A
  1. Acute insulin deficiency → unrestrained lipolysis → ↑blood FFA → ↑hepatic ketogenesis → ↑↑blood ketones (a fasting state response) → metabolic acidosis
  2. HyperGly → profound osmotic diuresis → dehydration + Na/K loss
  • 2o hyperaldosteronism → ↑↑K loss → net K deficit
  • Metabolic acidosis → H+/K+ intracellular shift
  • ↑↑Glc/ketones → hyperosmolar hyponatremia or normonatremia
46
Q

Clinical presentation of DKA

A

Clinical presentation: can be fulminant or mild but generally evolve rapidly

□ S/S of hyperglycaemia: polyuria, polydipsia, polyphagia, marked fatigue

□ S/S of dehydration/electrolyte disturbance: orthostatic hypotension or even shock

□ S/S of ketoacidosis:
→ Fruity smelling breath
→ Kussmaul’s respiration, leg cramps
→ Acute abdomen: diffuse abdominal pain, nausea, vomiting (due to ileus, usu only if severe acidosis)
→ Altered mentation: ↓consciousness, confusion, coma

47
Q

Diagnostic criteria of DKA

A

□ Hyperglycaemia: plasma glucose >14mmol/L
□ HAGMA: arterial pH <7.3, plasma HCO3- <15mmol/L ± ↑AG
□ Ketosis: moderate ketonuria or ketonaemia or ↑serum β-hydroxybutyrate (BHBA)

48
Q

First-line investigations for suspected DKA

A
  • Urine and plasma glucose
  • Urine ± plasma ketones or BHBA (urine ketone is useless)
  • Na, K, PO4 ± Mg
  • Anion gap (AG)
  • Urea, creatinine, Hb
  • ABG

If indicated, look for underlying cause:

  • CXR, ECG (MI)
  • Blood and MSU C/ST (Infection*)
  • Urine/serum osmolality (New DM)
  • PT, aPTT
49
Q

How to monitor DKA

A

Q1H:

  1. BP/P,
  2. RR,
  3. GCS,
  4. UO (Urine output)
  5. ± CVP (Central venous pressure)

Temperature - Q2H

Aspirate stomach if unconscious or vomiting ± ETT for airway protection if necessary

Foley’s catheter and set CVP as indicated

Abx if evidence of infection, treat hypotension and shock as appropriate

50
Q

Treatment of DKA

A

Rehydration - 1-2L 0.9% normal saline

  • Monitor serum Na
  • Keep under 10% body weight infusion over 12h
  • Watch out for fluid overload and CHF

Insulin - Regular human insulin

  • IV bolus + Infusion by insulin pump
  • Aim to decrease plasma glucose by 3-4mmol/L/h
  • change to dextrose-insulin when glucose is at 13mmol/L/h
  • Change to maintenance insulin when Anion Gap normalize

Potassium - 10-20mmol/h

  • Maintain serum K at 4-5mmol/L
  • due to acidosis and dehydration, K may appear normal

Sodium Bicarbonate

  • Only if pH under 7.0
  • Monitor serum K, maintain until over pH 7.0
51
Q

Hyperglycaemic Hyperosmolar State (HHS)

Which DM presents with HHS?

Which patients at high risk?

Pathogenesis?

A

Early T2DM with relative insulin deficiency

At risk: Elderly with difficulty drinking water, on diuretics, decreased sense of thirst, sudden copious intake of glucose-containing fluid

Pathogenesis:

Severe Hyperglycemia > osmotic diuresis exacerbated by insulin deficiency causing impaired tubular sodium reabsorption > Severe dehydration/ Hyperosmolarity

But no ketosis (unlike DKA): insulin still present + severe hyperosmolar state → suppress lipolysis

52
Q

Clinical presentation of hyperglycemic hyperosmolar state

A

Clinical presentation: typically insidious
□ Predisposition: Hx of ↓fluid intake or ingestion of large amounts of glucose-containing fluid

□ S/S of hyperglycaemia: polyuria, polydipsia, polyphagia, marked fatigue

□ S/S of dehydration/electrolyte disturbance: orthostatic hypotension or even shock

□ Neurological: focal neurological signs, seizures, general consciousness decrease, confusion, coma

53
Q

Diagnostic criteria of HHS

A

□ Hyperglycaemia: blood glucose >33mmol/L (different from DKA)

□ Non-ketotic: arterial pH >7.3, serum HCO3- >15mmol/L, mild ketonuria/ketonaemia only (complete opposite direction from DKA)

□ Hyper-osmolar: effective serum osmolality >320mOsm/kg (2[Na] + [Glc])

54
Q

Treatment of HHS

A

Rehydration with normal saline

Insulin: less aggressive than DKA, switch to maintenance insulin when alert, tolerating diet, osmo <315

55
Q

Investigations for HHS

A

Same as DKA panel

  • Urine and plasma glucose
  • Urine ± plasma ketones or BHBA (urine ketone is useless)
  • Na, K, PO4 ± Mg
  • Anion gap (AG)
  • Urea, creatinine, Hb
  • ABG

If indicated, look for underlying cause:

  • CXR, ECG (MI)
  • Blood and MSU C/ST (Infection*)
  • Urine/serum osmolality (New DM)
  • PT, aPTT
56
Q

Complications of HHS

A

Complications:
→ Risk of thrombosis esp in Caucasians + hyperosmolality
→ Risk of overshoot hypoglycemia and hypokalemia
→ Risk of cerebral oedema in children

57
Q

Precipitating factors of Hypoglycaemia in DM pt

A

□ Overtreatment: excessive insulin or insulin secretagogues (sulphonylureas or meglitinides)

□ Treatment with anti-diabetics precipitated by renal impairment

□ Insufficient carbohydrate intake

□ Excessive exercise

58
Q

Clinical presentation of Hypoglycaemia in DM pt

A

Adrenergic symptoms from ANS activity (usually occur first)
→ Palpitation, sweating, anxiety, tremor, tachycardia
→ Gradual decrease awareness in recurrent hypoglycaemia (eg. chronic DM)

Neuroglycopenic symptoms from ↓CNS activity due to hypoGly (usually occur later)
→ Hunger sensation
→ Periorbital and finger paraesthesia, seizures
→ Focal weakness, ↓sensation, clouding of vision
→ Depressed consciousness, drowsiness, coma

59
Q

Diagnostic criteria of Hypoglycaemia in DM pt

A

Whipple’s triad

□ Symptoms compatible with hypoglycemia
□ Low blood glucose coinciding with time of symptoms
□ Resolution of symptoms with correction of hypoglycemia

Table below is for DM patients, not normal people

60
Q

Treatment of hypoglycaemia in DM pt

A
  • Oral carbohydrates: sweet drink, early meal or snack, 15-20g oral glucose
  • IV dextrose if unconscious
  • IM glucagon if cannot obtain IV access
  • Monitoring: Haemstix Q1-2h until stable
    → duration depends on L/RFT and type of insulin/drug (in case of overdose)
61
Q

Prevention of Hypoglycaemia in DM pt

A

□ Education to keep good balance between exercise, meals and antidiabetic Tx
□ Revise glycaemic target if frequent asymptomatic hypoGly
□ Consider pre-emptive glucagon prescription for those at risk of level 2-3 hypoGly

62
Q

List Chronic Diabetic complications

A
63
Q

List diabetic eye complications

A

 Lacrimal system: ↓tear production

 EOM: CN III, IV, VI palsies (as part of mononeuritis multiplex)

 Lens: fluctuating refractive errors, cataract

 Glaucoma: idiopathic or due to rubeosis iridis

 Retina: retinopathy, papillopathy

 Others: ↑eye infections, ↑eye inflammation after ocular operations

64
Q

Subtypes of Diabetic retinopathy

A

□ Diabetic retinopathy (DMR): non-proliferative or proliferative

□ Diabetic macular oedema: retinal thickening and oedema involving macula
→ Can occur at any stage of DR
→ Commonest cause of vision loss in DM patients

65
Q

Risk factors of diabetic retionopathy

A

□ Long duration of DM: 80% have DMR after 20y of disease
□ Poor DM control
□ Vascular comorbidities, esp HTN, smoking
□ Others: pregnancy, rapid implementation of tight glycemic control

66
Q

5 pathophysiological processes of diabetic retinopathy

A

□ Retinal microangiopathy: chronic hyperGly → metabolic changes in retinal vessels → impaired vascular autoregulation → microaneurysm + retinal haemorrhage (‘dot-and-blot’)

□ Retinal ischaemia: endothelial damage → microthrombosis or occlusion → ischaemia → cotton wool spots (retinal nerve infarct) + venous beading (due to ischaemia) + intra-retinal microvascular abnormalities (IRMA) (anastomosis between arterioles and venules)

□ Breakdown of blood-retinal barrier: microangiopathy + microthrombosis → ↑capillary leakage → hard exudates (lipoprotein leakage) + macular edema (if occurring near macula) + retinal edema

□ Vasoproliferative substances: ischaemia → vasoproliferative factor secretion (eg. VEGF) → neovascularization (PDMR) + exacerbates ischaemia + breakdown of B-R barrier

□ Proliferative DMR: neovascularization w/ fragile vessels → vitreous haemorrhage

67
Q

5 severity levels of diabetic retinopathy

A
68
Q

Mild Non-proliferative diabetic retinopathy

  • Clinical finding
  • Treatment
A
69
Q

Moderate Non-proliferative diabetic retinopathy

  • Clinical findings
  • Treatment
A
70
Q

Severe non-proliferative diabetic retinopathy

Clinical finding

Treatment

A
71
Q

Proliferative diabetic retinopathy

Clinical findings

Treatment

A
72
Q

Macular edema

Clinical finding

Treatment

A
73
Q

Clinical presentation of diabetic retionopathy

A

Asymptomatic: majority with DMR shows no symptoms until very late stages

  1. Blurred vision of gradual onset: usually due to macular oedema
  2. Sudden visual loss indicates complications
    → Vitreous haemorrhage due to neovascularization into vitreous
    → Rubeotic glaucoma due to neovascularization of iris leading to acute angle closure
    → Tractional Retinal detachment due to fibrosis of abnormal vessels
74
Q

Diabetic nephropathy

Pathogenesis

2 histological types

A

Pathogenesis:
□ Mechanism: hyperglycaemia → ↑ROS production → chronic damage to glomerular epithelium
□ Histology:
→ Nodular glomerulosclerosis with Kimmelstiel-Wilson nodules
→ Diffuse glomerulosclerosis with ↑mesangial matrix

75
Q

Clinical presentation of diabetic nephropathy

Onset

A

□ Onset: microalbuminuria develops 5-15y after T1DM and 15-20y after T2DM dx

□ Albuminuria: slowly progressive from microalbuminuria (30-300mg/d) then to macroalbuminuria (>300mg/d)

□ Progressive CKD with gradual ↓GFR

76
Q

Management of diabetic nephropathy

A

□ CVD risk factors control: stop smoking…

□ Glycaemic control: aim A1c <7-8%
→ Prefer SGLT2i and GLP1a

□ BP control (esp by ACEI/ARB)

□ Treat hyperlipidemia (by statins or fibrates)

□ Renal replacement therapy if ESRD

77
Q

4 types of diabetic neuropathy

A

Acute diabetic mononeuropathy

Proximal diabetic neuropathy (diabetic amyotrophy, lumbosacral plexopathy)

Diabetic peripheral neuropathy

Diabetic autonomic neuropathy

78
Q

Acute diabetic mononeuropathy

  1. Cause
  2. Site
  3. Clinical presentation
  4. Management
A

□ Cause: likely ischaemic infarction of peripheral nerves

□ Site: most commonly CN III, CN VI, median and common peroneal palsies

□ Clinical presentation: acute onset, usually transient
→ Ptosis and divergent squint (CN III) (typically pupil-sparing)
→ Lateral rectus palsy (CN VI)
→ Upper facial and eye pain (ocular)
→ Foot drop (peroneal n.)

□ Mx: generally supportive but may require MRI to r/o stroke

79
Q

Proximal diabetic neuropathy

  1. Cause
  2. Site
  3. Clinical presentation
  4. Diagnostic test
  5. Management
A

□ Cause: likely ischaemic infarction of lumbosacral nerve roots and peripheral nerves

□ Site: asymmetrical, proximal, usually LL (but can affect UL)

□ Clinical presentation: progressive, typically transient, lasting weeks to months
→ Acute severe asymmetrical progressive proximal weakness and wasting
→ Hyperaesthesia and paraesthesia
→ Associated autonomic failure and weight loss

□ Dx: NCV (axonal degeneration), MRI pelvis (to r/o alternative causes)

□ Mx: 60% with good functional recovery in 12-24mo but mild residual weakness may remain
→ controlling underlying hyperglycaemia
→ Gabapentin/pregabalin/amitriptyline for neuropathic pain

80
Q

Diabetic peripheral neuropathy

Cause

Site

Clinical presentation

Screening tests (special)

Management

A

□ Cause: metabolic or osmotic neurotoxicity due to chronic hyperglycaemia

□ Site: symmetrical, distal, usually begins in LL

□ Clinical presentation:
→ Sensory polyneuropathy: glove-and-stocking sensory loss of all modalities or paraesthesia
→ Motor polyneuropathy: ↓tendon reflexes in LL ± weakness, wasting (generally later)
→ Skin and joint: foot ulcers, foot deformities, Charcot arthropathy

□ Screening: by symptoms and monofilament (small fibre) and tuning fork (large fibre) tests

□ Workup: clinical ± NCV study and blood test (to r/o alternative causes, eg. B12)

□ Mx:
→ Optimize glycemic control as mainstay
→ Gabapentinoids (gabapentin/pregabalin) and antidepressants (amitriptyline) for pain

81
Q

Cardiovascular manifestation of diabetic autonomic neuropathy

A

Impaired CO control: resting tachycardia (early), failure of exercise-induced ↑HR resulting in exercise intolerance

Orthostatic hypotension due to central/peripheral sympathetic denervation

Postural tachycardia with lightheadedness, dizziness, presyncope

82
Q

Sudomotor and vasomotor manifestations of diabetic autonomic neuropathy

A

 Distal hypohidrosis with compensatory proximal hyperhidrosis (abnormal excessive sweating)

 Thermoregulatory impairment and hyperthermia

 Diabetic dermopathy (dryness, itching) and Charcot arthropathy

83
Q

Gastrointestinal manifestation of Diabetic autonomic neuropathy

A

 GERD
 Gastroparesis: N/V, early satiety, bloating, upper abd pain
 Diarrhoea: painless watery nocturnal diarrhoea

84
Q

Genitourinary manifestation of Diabetic autonomic neuropathy

A

 Bladder dysfunction: ↓ability to sense full bladder, incomplete emptying, recurrent UTI, overflow incontinence

 Ejactulatory dysfunction: retrograde ejaculation, erectile dysfunction

 Dyspareunia due to ↓vaginal lubrication

85
Q

Diabetic foot ulcer

Cause

Complications

Risk factors

A

Cause: Diabetic peripheral neuropathy

Common manifestation:
□ Foot ulcers: 25% lifestyle risk, annual risk 2%/y
□ Diabetic foot infections: cellulitis, osteomyelitis

RFs of foot ulcer development:
□ Previous foot ulceration (most important)
□ Neuropathy (80%): loss of monofilament sensation, neuropathy disability score
□ Foot deformity
□ Concomitant vascular disease

86
Q

Management of diabetic foot

A

General foot care recommendations:
□ Annual comprehensive foot examination to identify RFs incl inspection + palpation of pulses
→ Refer vascular surgery for patients with significant claudication or +ve ABI

□ General foot self-care

□ Multidisciplinary approach (refer podiatry)

87
Q

Diabetic neuropathic (Charcot) Arthropathy

Pathogenesis

A

Pathogenesis:

Lack of proprioception + ligament laxity + joint instability + deformity → prone to damage by minor trauma

vasomotor changes due to autonomic neuropathy lead to exaggerated local inflammatory response → arthropathy

88
Q

Clinical features of Diabetic neuropathic arthropathy

A

Clinical features: generally painless
□ Acute arthritis: sudden onset unilateral warmth, erythema, swelling over foot/ankle (often ppt by minor trauma)
→ Joint involved: tarsal/TMTJ > MTPJ/ankle

□ Chronic arthritis: slowly progressing arthropathy with insidious swelling ± acute attacks

□ Foot deformity: collapse of midfoot arch, bony prominences in peculiar places ± pressure ulcerations

89
Q

Xray features of Diabetic Neuropathic (Charcot) Arthropathy

A

□ Early: soft tissue swelling, loss in joint spaces

□ Late: forefoot bone resorption, disappearance in MT heads, pencil-pointing of phalangeal/MT shafts

□ Complication features: stress fractures, subluxation/dislocations

90
Q

Management of Diabetic Neuropathic (Charcot) Arthropathy

A

□ Short-term immobilization (3-6mo): proven to ↓long-term joint damage and progression

□ Consider antiresorptive agents (bisphosphonates, calcitonin) as adjunct

□ Orthopaedic surgical correction in severe cases

MBBS VI - SpC - Medicine (80 decks)

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