Diabetes Mellitus -2 Flashcards

1
Q

DKA - Acute Complication

A

Occurs in type 1 DM or type 2DM who have high levels of anti-insulin caused by intercurrent illness - rare in type 2

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2
Q

Causes of DKA

A

*Missed insulin
*Relative insulin deficiency
stress, steroid therapy, infection
*Tissue damage : trauma, operation, burns, shock, stroke, MI
*Pregnancy, labor & lactation
↑ ketone bodies Formation : as in Starvation, severe exertion or excess fat intake

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3
Q

Clinical Picture of DKA

A

*Symptoms of uncontrolled DM
*Respiratory - Kussmaul respiration which is deep and rapid
*Acetone breath
*Patient becomes unconcious

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4
Q

Systemic symptoms of DKA

A

Cardiovascular symptoms: shock - due to polyuria, peripheral vascular disease, dysrhythmias, Dehydration

Kidney :
Ketonuria + glucosuria, severe polyuria, polydypsia and dehydration (dry inelastic skin, sunken eye, thirst, low BP & low temp)

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5
Q

Systemic symptoms of DKA - GIT, Muscular, End Stage

A

GIT:
Acute abdomen (epigastric pain), Nausea, vomiting, constipation & hematemesis

Muscles:
Generalized weakness & muscle pain due to absence of energy.

End stage:
coma (due to acidosis, ketosis, dehydration & electrolyte imbalance)

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6
Q

Complications of DKA

A

Adult respiratory disorders syndrome (ARDS,)
DIC, arterial and venous thrombosis,
Pancreatitis,
Brain edema

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7
Q

Investigations for DKA

A

Blood
-Blood sugars: Hyperglycemia, ketonemia
- Blood pH : Acidosis (decreased plasma HCO3) dehydration leads to ↑ PCV, ↑ serum creatinine c-T FFA & TG
- Serum K: normal or high despite depletion of body K due to extracellular shift
leucocytosis and ↑ serum amylase (for pancreatitis)
- Full blood count
Euglycemic ketosis: when blood glucose is normal
* Urine: glucosuria, ketonuria (to check Rx response), polyuria
ECG (To check for hypokalemia, tall QRS wave),
chest X-ray

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8
Q

Treatment Aim

A
  • Confirm diagnosis
  • Search for and treat any precipitating cause
  • Assess hydration status and give fluid
  • Give insulin
  • Monitor clinical signs and biochemistry
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9
Q

Fluid replacement

A
  • Hospitalization better in ICU
  • Fluid replacement:
    Amount: guided by CVP - by central venous catheter (10cm H2O ideal)
    *1 L / hour till HR & BP return to normal - monitor blood sugar.
    *Type of fluid:
    At 1st: isotonic saline
    Then: dextrose 5% when blood glucose drops < 14 mmol/l (to avoid hypoglycemia from insulin admin). In KATH if the patient is still hypovolemic 5% dextrosaline is given, then freq. of insulin given is reduced.
    –Hypotonic saline with hypernatremia
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10
Q

Insulin Rx for DKA

A

Insulin
Type: soluble/short acting
Dose: low dose regimen 0.1 U / kg / h. continuous infusion via insulin pump or deep IM.
Follow up: by blood sugar every hour & give further insulin accordingly.

In KATH - Give bolus of insulin - IV 10U soluble + IV 10U subcutaneous. Continue monitoring blood sugar till <14mmol/l, put on dextrose and reduce freq. of insulin.

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11
Q

Treatment of acid base and electrolyte disturbances - DKA

A

Shouldn’t always be done, but if patient has the following: *Metabolic acidosis : -+ NaHCO3.
Indication : in severe case
Clinical : Kussmaul respiration),
Lab.: pH < 7.1 & HC03 <10 mEq
Dose: 1 L of 1/6 molar NaHC03 IV (till PH > 7.2 not reach 7.4 to avoid over correction -> Alkalosis)

*Correct plasma K+ level:
K from the start Hypo K+ : occurs with insulin treatment due to intracellular shift
Dose: Add 10 ml KCL (20 mEq) to each 1 L of fluid given. Oral given after recovery

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12
Q

Care for comatose patient, treat cause and precipitating factors & monitor

A
  • Care of comatose Pt.:
  • Treat cause & precipitating factors
  • Monitoring: state of hydration, urine output, conscious level, plasma glucose, K and ABG
    Blood culture, urine culture and chest xray
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13
Q

Care for comatose patient, treat cause and precipitating factors & monitor

A
  • Care of comatose Pt.:
  • Treat cause & precipitating factors
  • Monitoring: state of hydration, urine output, conscious level, plasma glucose, K and ABG
    Blood culture, urine culture and chest xray
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13
Q

Care for comatose patient, treat cause and precipitating factors & monitor

A
  • Care of comatose Pt.:
  • Treat cause & precipitating factors
  • Monitoring: state of hydration, urine output, conscious level, plasma glucose, K and ABG
    Blood culture, urine culture and chest xray
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14
Q

Othe Rx of DKA

A

Take blood sample, give broad spectrum antibiotic, Prophylactic antibiotic.
* Nasogastric tube: to aspirate gastric content - so it won’t aspirate (pneumonia, pneumonitis)
*Heparin IV in old and dehydrated patients to guard against DIC (Because of dehydration and hypovolemic state)
*Frusemide IV in oliguric patients
*O2 if P02 < 80mmHg

*Continue with Insulin therapy
* Prevent recurrence: Avoid reduction of insulin dose during intercurrent illness (when insulin resistant)

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15
Q

Hyperglycemia hyperosmolar non-ketotic state causes

A

Occurs in old type 2 DM due to (infection. MI). 55mmol/l blood sugar
- Absence of fat reserve or fat mobilization (relative lack of GH or cortisol)
- Insensitive thirst center in old age led to dehydration aggravated by use of diuretics.
Be careful of the amount of insulin you give - you’ll push them into hypo.

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16
Q

Precipitative factors of HHNK state

A

Infection
Infarction

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16
Q

Clinical presentation of HHNK state - PPD + Neuro symptoms

A

Severe polyuria, polydipsia & dehydration

*No or little ketosis
* Prerenal uremia may occur due to dehydration
Neurologic symptoms: convulsions, coma, hemiparesis, stupor

17
Q

Investigations for HHNK

A

Investigations
Blood (Culture):
* severe hyperglycemia often > 55mmol/l
* ↑ PCV, ↑ Na, ↑ plasma osmolality (N. 290 mosm/L)  Urine: glucose without ketone bodies

18
Q

Treatment of HHNK

A

Treatment : Same as DKA but without bicarbonate
Fluids
Type : 1/2 normal saline (1/2 molar) - Give ordinary normal saline.
Amount : IL / hour not faster to avoid cerebral edema
Insulin : smaller amount than ketoacidosis (stat dose)
Heparin : since there is ↑ incidence of DIC

19
Q

Chronic Complications - Macrovascular (Affect brain and heart)

A

Diabetes is a risk factor for developing atherosclerosis.

20
Q

Other Risk Factors for development of macrovascular complications:

A
  • Duration of diabetes
  • Increasing age
  • Systolic hypertension
  • Hyperinsulinaemia due to insulin resistance (type 2)
  • Obesity and syndrome X (metabolic syndrome)
  • Hyperlipidaemia (particularly hypertriglyceridaemia/low HDL
  • Proteinuria (including microalbuminuria) 

21
Q

Heart complication of DM

A

Coronary heart disease

  • Myocardial infarction is three to five times more among diabetic people
  • Women with diabetes lose their premenopausal protection from coronary artery disease.
  • Painless angina and myocardial infarction may be due to neuropathic damage to the autonomic nerves serving the myocardium.
  • Atypical presentation of angina and myocardial infarction (malaise, sweating, dyspnea and syncope which may be confused with hypoglycemia
22
Q

Why is long term mortality from MI increased in diabetes?

A

Due to increased risk of Heart Failure in Diabetes.

23
How is MI managed in a diabetic patient?
Management is similar to non- diabetic population with more caution with usage of thromolytic therapy because of the risk of intraocular haemorrhage in the patient with retinopathy.
24
Diabetes and Caardiomyopathy + Main feature
* Diabetes can cause a cardiomyopathy even without coronary artery atheroma. * Left ventricular contractility abnormalities detected by echocardiology is the main subclinical feature.
25
Hypertension and Diabetes
Hypertension is twice more in diabetes than non-diabetic. * Closely associated with metabolic syndrome X, insulin resistance or hyperinsulinaemia
26
How does hyperinsulinemia lead to hypertension?
Through * Stimulation of kidney reabsorption of sodium and water. * Stimulation of calcium and sodium in the vascular smooth muscle which enhance contractility causing hypertrophy of vascular smooth muscle, and stimulation of sympathetic nervous systems.
27
Why is the control of hypertension in diabetes important?
* Hypertension is a major CVS risk factor. *Hypertension can accelerate microvascular complication as nephropathy and retinopathy.
28
How to investigate hypertension in diabetes?
Investigate pt's for * Secondary hypertension (Cushing’s, Conn's disease and Pheochromocytoma) * Renal damage (proteinuria or microalbuminuria, urine microscopy, serum creatinine and electrolytes) * CV damage (ECG, chest x-ray for left ventricular hypertrophy) * Other CV risk factors eg. hyperlipidemia, poor glycemic control
29
Treatment of HPT in Diabetes
ACE inhibitors are the first choice because: 1. It delays the progression of diabetic retinopathy and reduces microalbuminuria. 2. A thiazide should be used at low dose to avoid worsening of glycemic control and aggravation of dyslipidemia. 3. Beta-adrenoceptors can aggravate hyperglycemia, dyslipidemia and impotence.
30
Peripheral arterial disease and Diabetes - symptoms
- Asymptomatic - Intermittent claudication (calf pain on walking) - Buttock pain may occur if iliac vessels are affected - Decreasing claudication distance and rest pain denote critical ischemia - Unhealed skin wound
31
Peripheral arterial disease and Diabetes - Signs
- Absence of pedal pulse ( 8% dorsalis pedis, 2% posterior tibialis) - Cold extremities - Pale or bluish color of the skin - thin, shiny skin with scanty hair - dystrophic toenail
32
Investigations for Peripheral artery disease
- Doppler US - Ankle Brachial Index (ABI) : normal value 0.98 - 1.31 - Angiography
33
Prevention of macrovascular complication
- Early control of blood glucose - Strict control of hypertension. - Stop smoking - Treatment of lipid abnormalities: to the lowest achievable level - ACE inhibitors /angiotensin II receptor antagonists: 25–35% lowering of the risk of heart attack, stroke, overt nephropathy or cardiovascular death - Low dose aspirin: can reduce macrovascular risk, but is associated with a morbidity and mortality from bleeding.
34
Cerebral stroke and Diabetes (macro)
- Stroke is twice higher in diabetic population than non-diabetics - Mortality and disability from stroke are also worse in the diabetic person compared to non- diabetic people (May because of elevation of blood glucose level following stroke)
35
The Danger sites of Microvascular complications - Diabetes Mellitus
Retina Renal Glomerulus Nerves
36
Classification of Diabetic Neuropathies
* Focal and multifocal neuropathies e.g. mononeuropathy, amyotrophy, radiculopathy, entrapment neuropathy, mononeuritis multiplex. * Symmetrical neuropathies e.g. diabetic peripheral neuropathy and autonomic Neuropathy * Cranial nerve palsies (III, IV, VI & VII)
37
Mononeuropathies + Peroneal nerve palsy
Affect (single nerve) peroneal, median or ulnar nerves. It tends to occur at sites of entrapment (wrist) or external compression. * Peroneal nerve palsy is characterized by weakness or paralysis of foot and toe dorsiflexors, foot drop and foot eversion. * Impaired sensation over the dorsum of the foot and the lower anterior aspect of the leg. *The ankle reflex is preserved as is foot inversion.
38
Entrapment neuropathies
1-Carpal tunnel syndrome: found in 5.8 % of diabetic patients. It has a less favorable outcome after surgical decompression, as diabetes slows nerve regeneration. 2- Ulnar neuropathy at the elbow affects 2.1% of diabetic patients 3- Peroneal neuropathy at the fibular head affects 1.4–13% of diabetic patients. 4- Lateral cutaneous nerve of the thigh (meralgia paresthetica) affect 0– 1.0% of diabetic patients.
39
Clinical Features of autonomic neuropathy
* Impotence * Postural hypotension (giving dizziness and syncope) * Resting tachycardia or fixed heart rate * Gustatory sweating—sweating after tasting food * Dysphagia with delayed gastric emptying, nausea/vomiting * Constipation or diarrhea * Urinary retention or overflow incontinence * absent sweating on the feet (anhidrosis). This increases the risk of ulceration. * Abnormal pupillary reflexes
40
Assessments for diabetic neuropathy
Annually check the following: * Lying and standing BP (measure systolic BP 2 minutes after standing; normal is difference <10 mmHg drop, >30 mmHg is abnormal) * Pupillary responses to light
41
Other less common tests for diabetic neuropathy if the diagnosis is uncertain or in high-risk patients.
* Loss of sinus arrhythmia: Measure inspiratory and expiratory heart rates after 5 seconds of each (<10 beats/min difference is abnormal,>15 are normal). * Loss of heart rate response to Valsalva maneuver: Look at the ratio of the shortest R–R interval during forced expiration against a closed glottis compared to the longest R–R interval after it (<1.2 is abnormal). * BP response to sustained hand-grip: Diastolic BP prior to the test is compared to diastolic BP after 5 minutes of sustaining a grip equivalent to 30% of maximal grip. A diastolic BP rise >16 mmHg is normal, <10 mmHg is abnormal. A rolled-up BP cuff to achieve the required handgrip may be used.