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CVS + GIT?? Flashcards

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1
Q

Define hypertension.

A

A sustained and elevated BP above 140 systolic and 90 diastolic.

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2
Q

Identify the classification categories of hypertension.

A

Normal <120 S <80 D
High normal 120 - 139 S 80 - 89 D
Grade 1 (mild) 140 - 159 S 90 - 99 D
Grade 2 (moderate) 160 - 179 S 100 - 109 D
Grade 3 (severe) > 180 S >110 D

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3
Q

Identify the risk factors associated with hypertension.

A

Family history
Race
Age (DBP increases 50- then decreases 60+, SBP
increases throughout life)
Salt (Na+) intake
Smoking
Obesity (central adiposity -> hypertension)
Alcohol (3+ drinks/day increases risk)
Low dietary K+ (increased Na+ elimination)

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4
Q

Distinguish between primary and secondary hypertension.

A

PRIMARY
90% cases have no clear aetiology
Disruption of complex interactions of mechanisms that regulate BP

SECONDARY
10% cases
Results from other disorders – e.g. drugs, renal disease, adrenal issues, congenital inheritance, metabolic disorders

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5
Q

Describe the pathophysiological processes possibly involved in the development of primary hypertension.

A

Sympathetic Nervous System
Increased SNS activity -> Increased HR and systemic vasoconstriction -> Increased BP

RAAS
Moderates vascular tone, influences sodium (Na) and H2O retention

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6
Q

Summarise nonpharmacological treatment strategies for hypertension.

A

↓ Weight
↓saturated and total fats, eat more
vegetables and fruit
5 – 20 mm Hg/10 kg lost

↓ Na+
≤ 6 g Sodium Chloride per day
2 – 8 mm Hg

↑ Exercise
Regular aerobic activity (brisk walking) 30 min per day
4 – 9 mm Hg

↓ Alcohol
≤ 2 drinks/day for men ≤ 1 drink/day for women
2 – 4 mm Hg

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7
Q

Summarise pharmacological treatment strategies for hypertension.

A

ACEIs (inhibits formation of Angiotensin II)
ARBs (block angiotensin receptors)
Alpha (α) Blockers (arterial vasodilators)
Beta (β) Blockers
Calcium (Ca++) Channel Blockers
Diuretics (↓ Na+ reabsorption)

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8
Q

Discuss why adhering hypertension medications is

important.

A

With proper therapy, the risks of long-term complications can be minimized, resulting in a longer and healthier life.

Medications don’t cure only control symptoms.

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9
Q

Identify the impact of chronic hypertension on the heart.

A 
Can result in heart disease
Increased afterload
Accelerates atherosclerosis of coronary arteries
Left ventricular hypertrophy
Systolic dysfunction
Coronary artery disease
Arrhythmia
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10
Q

Identify the impact of chronic hypertension on the kidneys.

A

Hyaline accumulates in the wall of small BV narrowing the lumens which causes ischemia leading to tubular atrophy, internal fibrosis and glomerular alterations.

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11
Q

Identify the impact of chronic hypertension on the brain.

A

Risk factor of stroke
Hemorrhagic CVA : rupture of intracerebral vessels
Atherothrombotic CVA : due to atherosclerotic plaque
Lacunar infarcts
Slit haemorrhage

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12
Q

Identify the impact of chronic hypertension on the retinas.

A 
Hypertensive retinopathy
Vision problems
Rupture of retinal vessels
Haemorrhage
Exudation of plasma lipids
Papilledema
Copper wiring
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13
Q

Identify the impact of chronic hypertension on the arteries.

A

Atherogenesis -> degeneration of walls
Hyaline arteriosclerosis
Hyperplastic arteriosclerosis

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14
Q

4 common drug groups of hypertension treatment

A

A - angiotensin converting enzyme inhibitors
(ACEI), angiotensin receptor blockers (ARB),
alpha blockers (A1B)

B - beta blockers (BB)

C - calcium channel blockers (CCB)

D - diuretics (D)

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15
Q

Outline the method used to determine what medication to use when treating hypertension.

A

First choice

  • ACE inhibitor
  • Calcium channel blocker
  • Low dose thiazide diuretic

Second choice

  • ACE inhibitor + calcium channel blocker
  • ACE inhibitor + low dose thiazide diuretic

Third choice
- ACE inhibitor + calcium channel blocker + low dose thiazide diuretic

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16
Q

Explain the mode of action of ACEIs

A

Inhibits formation of Angiotensin II

↓ Angiotensin II-mediated vasoconstriction and aldosterone mediated volume expansion → ↓BP

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17
Q

Explain the mode of action of ARBs

A

Block angiotensin receptors

Similar to ACEI’s

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18
Q

Explain the mode of action of Alpha (α) Blockers

A

Arterial vasodilators

Not first line drugs for hypertension due to risk of hypotension and cardiac problems.

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19
Q

Explain the mode of action of Beta (β) Blockers

A

Blocks action of SNS on β1 receptors of heart

• ↓HR, ↓contractility→↓CO
• Suppresses reflex tachycardia
• Blocks β1 receptors in kidney→ ↓renin (RAAS)→
↓vasoconstriction→ ↓resistance

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20
Q

Explain the mode of action of Calcium Channel Blockers

A

Disrupts movement of Ca++ ions through membrane
channels of smooth/cardiac muscle cells

• ↓intracellular calcium, ↓cardiac contractility
• ↓ Ca++ results in ↓contraction of vascular smooth
muscle→ ↑vasodilation, ↓PVR, ↓BP

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21
Q

Explain the mode of action of Diuretics

A

↓ Na+ reabsorption

Thiazides:
• Produce moderate diuresis and ↓ vascular resistance

High Ceiling Loop (potent) :
• Large diuresis generally for conditions such as pulmonary oedema rather than hypertension

K+ Sparing:
• Mild diuresis

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22
Q

Define primary hypertension

A

Primary hypertension is the result of complex interaction of genetic and environmental factors which disrupt normal BP regulating mechanisms leading to increased blood volume, SNS activity, activity of the RAA system, and renal Na+ retention.

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23
Q

Regulation of blood pressure

A

BP = Cardiac output (CO) * Peripheral Resistance

Neural Control (Rapid acting short duration)-
 - Baro-receptors → ANS → regulation of CO and 
   vasoconstriction

Hormonal Control (slow acting long duration)-
• Renin-Angiotensin → vasoconstriction
• Aldosterone → Na+ and water retention → increased blood volume → increased CO
• Catecholamine (adrenaline) → vasoconstriction
• Prostaglandins and Nitric oxide (NO) → vasodilation
• Atrial Natriuretic hormone → vasodilation

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24
Q

Define atherosclerosis

A

A common form of arteriosclerosis which arises due to a thickening and hardening (loss of elasticity) of the arterial wall.

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25
Q

Identify the risk factors for atherosclerosis

A 
Hypertension  (2x risk)
Smoking
High dietary intake of cholesterol and saturated fats
Diabetes mellitus
Obesity and sedentary lifestyle
Toxins
Virus
Immune reaction
Older age
Gender
Genetics
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26
Q

Describe where atherosclerosis most commonly occurs

A

Coronary arteries and cerebral arteries

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27
Q

Describe steps in development of atherosclerosis

A
  1. Chronic endothelial injury
  2. Increased endothelial permeability and inflammatory cell migration
  3. Lipid accumulation and smooth muscle cell proliferation
  4. Plaque formation
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28
Q

Explain how cholesterol transport around the body contributes to atherosclerosis

A

.

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29
Q

Describe clinical manifestations of atherosclerosis

A
  • Pain anywhere that has a blocked artery
  • Shortness of breath
  • Fatigue
  • Confusion if blockage affects circulation to brain
  • Muscle weakness in legs from lack of circulation
  • Chest pain or angina
  • TIA
  • Inadequate tissue perfusion
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30
Q

Describe pharmacological treatments for atherosclerosis

A

Considered when lifestyle changes are ineffective

Statins (HMG-CoA reductase inhibitors)
Inhibition HMG-CoA reductase →↓ cholesterol production

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31
Q

Define aneurysm

A

Swelling of an arterial wall due to weakness from trauma, infection, congenital defect or atherosclerosis

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32
Q

Describe the aetiology of aneurysms

A 
Risk factors:
 smoking tobacco
    hypertension, or high blood pressure
    poor diet
    inactive lifestyle
    obesity
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33
Q

What are the classifications of aneurysms

A

Aortic aneurysm
Cerebral aneurysm
Peripheral aneurysm

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34
Q

Describe types of emboli and associated risks

A

FAT
associated with severe fractures
fat globules enter venous sinus & lodge in pulmonary vasculature

AIR
decompression sickness
nitrogen comes out of plasma due to pressure changes

35
Q

Explain risk factors for thrombus formation in arterial and venous vasculature

A

Arterial – age, hypertension, diabetes, recent heart failure, previous stroke, prosthetic valves

Venous – DVT, pulmonary embolism

36
Q

Discuss the progression of coronary heart disease to acute myocardial infarction, including manifestations, diagnostic evaluation of myocardial infarction and management.

A
  • Obstruction of coronary arteries
  • Myocardial oxygen demand > myocardial oxygen
    supply for more than 20 min
  • Heart uses oxygen supply, then breaks down
    glycogen stores
  • Reduces ATP production & produces lactic acid
  • Acidosis = decreased myocardial function
  • Decreased ATP = unstable Na+/K+ pump = disrupts
    depolarisation/repolarisation of cardiac cells
  • Loss of contractile function
  • Myocytes are irreversibly damaged = cell death =
    tissue death
37
Q

Describe the inflammatory response in the post infarction recovery period and the long-term effects this may have.

A

???

Inflammation has crucial role in clearing the infarct of dead cells and extracellular matrix debris

38
Q

Describe the most common drugs used in angina and MI and their actions.

A

.

39
Q

Discuss the progression of coronary heart disease to acute myocardial infarction, including manifestations, diagnostic evaluation of myocardial infarction and management

A

.

40
Q

Adverse effects of statins

A

Mild muscle injury (aches, tenderness, weakness)
Hepatotoxicity
Liver injury

41
Q

Complications of Atherosclerosis

A

Arterial plaques lead to occlusion causing coronary heart disease, peripheral vascular disease and cerebrovascular disease

  • Arterial weakening → aneurysm and rupture
  • Thrombus formation → acute occlusion/embolism
42
Q

Causes of embolisms

A

Thrombi normally adhere to vessel wall, however may break away to form distal lodged emboli.

Atherosclerosis frequent cause of arterial thrombi/emboli

43
Q

Development of thrombi

A

Usually requires 2 of 3 conditions described by Virchow’s triad to be present

  • endothelial injury
  • abnormal blood flow
  • hypercoagubility

Stasis of blood
Increased blood coagulability
Vessel wall injury
Deep vein thrombosis (DVTs)

44
Q

Discuss the manifestations of myocardial infarction

A 
Pressure / tightness in chest
Shortness of breath
sweating
nausea
vomiting
anxiety
cough
dizziness
increased HR
upper back pain
light-headedness
jaw pain
45
Q

Discuss the diagnostic evaluation of myocardial infarction

A

.

46
Q

Discuss the management of myocardial infarction

A

M – Morphine (for pain) – plaque fissuring & thrombus propagation

O – Oxygen – Increased O2 sat of haemoglobin

A – Aspirin – Antiplatelet agent, inhibits prostaglandin thromboxane A2

N – Nitrates – vasodilating, decreased venous return & BP, decreased O2 consumption

Coronary bypass (stent) if needed – increases blood flow

47
Q

Define angina pectoris

A

Crushing or choking pain in the anterior chest wall and radiating into the left arm or neck

Classification:

  1. Classical or stable angina
  2. Variant (vasospastic) angina
  3. Unstable angina
48
Q

Apart from an increased risk for myocardial infarction, what are other complications of atherosclerosis?

A

As weakens the arterial wall and therefore increases the probability of aneurysm formation.

As in the lower limb (peripheral vascular disease) can be sufficiently severe to cause skin and sensory changes and eventually necessitate amputation if blood flow is not improved via interventions such bypass grafts.

As increases the risk of thrombus formation and embolism

49
Q

Discuss the use of statins.

A

A reduction in cholesterol will prevent the progression of
atherosclerosis and reduce the risk of thrombus formation.
Statins are the best drugs to reduce cholesterol.

They act as HMG-CoA (hydroxy-3-methylglutaryl coenzyme A) Reductase Inhibitors reducing the amount of cholesterol made by the liver and decreases LDL levels. However, some controversy regarding their ability to improve mortality rates exists.

50
Q

Describe the progress of coronary heart disease to myocardial ischaemia. (TUT)

A

The early stages of coronary heart disease begin with non-symptomatic atherosclerosis.

As the size of the plaque increases the person may experience stable angina, where the chest pain related to myocardial ischaemia occurs on exertion and ends with rest.

As the plaque grows and becomes fissured, the person may experience unstable angina because intermittent thrombus formation causes the myocardial ischaemia and chest pain to occur on rest.

The next step in the continuum is myocardial infarction (ST elevation myocardial infarction or non-ST elevation myocardial infarction), where the ischaemia is sustained and causes death of myocytes. If the infarction is severe enough, heart failure and cardiogenic shock may occur.

51
Q

Describe the pathophysiology of a myocardial infarction

A 
Myocardial infarction (myonecrosis) occurs when myocardial oxygen demand exceeds myocardial oxygen supply for a sustained period, usually about 20 minutes.
This is usually due to obstruction of the coronary arteries by atherosclerotic plaque and thrombi, and/or vasoconstriction, although it is possible for an infarction to
occur in diseases where there is a very high oxygen demand such as in thryotoxicosis.

As oxygen demand outstrips supply the heart muscle uses up its oxygen supply and then breaks down its glycogen stores and converts to anaerobic metabolism, which greatly reduces ATP production and produces a lactic acid byproduct. The acidosis affects myocardial function.

The inability to make sufficient ATP impacts on the function of the sodium–potassium ATP pump, which in turn disrupts normal depolarisation and repolarisation of cardiac muscle cells, leading to loss of contractile function in the affected cells. After about 20 minutes of ischaemia the myocytes become irreversibly damaged, and die.

52
Q

Detail complications associated with the period after infarction.

A

The major complications associated with myocardial infarction are sudden death from life-threatening arrhythmias and heart failure and cardiogenic shock.
Arrhythmias occur because damaged cells are leaky cells, and they can leak at a faster rate than the pacemaker cells in the SA node. This allows ectopic pacemakers (an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart) to develop.

Also damage to the conduction pathway can change the path that the impulse takes and cause re-entry phenomena where an impulse can’t pass through the
normal pathway due to delayed repolarisation but then spreads to myocytes via a different pathway and returns through the normal pathway in the wrong direction.

In some instances the pathway can be completely blocked and the atria may beat independently to the ventricles. In addition when a large chunk of myocardium is noncontractile due to ischaemia or infarction, this greatly reduces the ejection fraction and cardiac output, which can cause heart failure and shock.

53
Q

What non-pharmacological treatment interventions may be initiated post MI?

A

RIB

Reperfusion therapy:
The goal of reperfusion therapy is to restore blood flow through the blocked coronary artery and is the most effective way preserve myocardial function and limit infarct size.

Fibrinolytics
Activate plasminogen to convert into plasmin which digests fibrin meshwork holding clots together.

Revascularisation therapy:
In the coronary artery bypass grafting procedure, one end of a segment of healthy blood vessel is grafted onto the
aorta, and the other end is connected to the diseased coronary artery at a point distal to the region of atherosclerotic plaque. The graft, therefore, constitutes a shunt that allows blood flow to circumvent the occluded section of a diseased coronary vessel.

54
Q

What discharge advice and information would you provide

if someone had been diagnosed with unstable angina

A

Lifestyle modifications – diet exercise, stop smoking, if
diabetic good BSL control

Education on use of nitroglycerin, keep in dark bottle out
of sun and discard after 90 days

55
Q

How does alteplase rapidly treat chest pain? Why is

timing of its administration important?

A

Alteplase and streptokinase are thrombolytic drugs which indirectly convert plasminogen to plasmin which then digests the fibrin meshwork of clots. Therefore the aim is to rapidly dissolve the thrombus (blood clot) blocking the patient’s coronary arteries, & restore blood flow.

56
Q

How does aspirin reduce reoccurrence of thrombosis?

A

Aspirin inhibits cyclooxygenase, the enzyme needed
for formation of prostaglandins and also thromboxane.
At low doses, only thromboxane A2 is inhibited, reducing platelet aggregation.

57
Q

Explain why heparin is useful in the treatment of myocardial infarction. Indicate why warfarin is unlikely to be beneficial in the acute phase of myocardial infarction

A

Heparin may have been useful because it enhances the activity of anti-thrombin which is able to inactivate thrombin and factor X (and therefore reduce clotting).

The mode of action of warfarin is associated with the blockade of clotting factor synthesis particularly factor X and prothrombin. These substances require vitamin K for their synthesis and warfarin is a vitamin K antagonist.

The peak effectiveness of Warfarin is delayed once dosing commences because warfarin can only block clotting factor synthesis but not affect existing clotting
factors.

Therefore in the acute period if there was concern about preventing further thrombus growth in the patient warfarin would not be the drug of choice, as its action is too slow.

58
Q

What are the risks associated with not taking hypertensive medications?

A

Left untreated, hypertension can lead to heart disease, kidney disease, and stroke. Conversely, a treatment program of lifestyle modifications and drug therapy can reduce BP and the risk of long-term complications. The degree of injury is directly related to the degree of pressure elevation: The higher the pressure, the greater the risk.

Among people 40 to 70 years old, the risk of cardiovascular disease is doubled for each 20 mm Hg increase in systolic BP or each 10 mm Hg increase in diastolic BP, beginning at 115/75 mm Hg and continuing
through 185/155 mm Hg.

59
Q

Describe the 3 forms of diabetes mellitus.

warning long

A

What happens?
1 - Pancreas fails to produce enough insulin. Loss of insulin-producing beta cells in islets of Langerhans in pancreas = loss of glycaemic control. Sudden onset
2 - Insulin resistance. Cells do not respond to insulin properly. Lack of insulin may also develop – beta cell destruction as disease progresses. Gradual onset
G - Pregnant woman with no previous DM history develops high blood sugar levels. Glucose intolerance in pregnancy

Prevalence
1 - ~10% DM
2 - ~90% DM
G - Up to 8% in Aust

Length of DM
1 - Lifetime
2 - lifetime
G - Can progress to Type 2 DM

Body size
1 - Thin or normal
2 - often obese
G - prego

Symptoms
1 - Increased BSL
  - Polydipsia
  - Polyuria
  - Polyphagia
  - Weight loss
  - Blurry vision
  - Fatigue
  - Low BSL
  - Sweating
  - Shakiness
  - Weakness
  - Hunger
  - Confusion
2 - Polyphagia
   - Polyuria
   - Polydipsia
   - Fatigue
   - Blurry vision
   - Sores or cuts that won’t heal
G - Usually no symptoms.
    - Polydipsia
    - Polyuria
    - Fatigue
    - Nausea and vomiting
    - Bladder infections
    - Yeast infections
    - Sugar in urine
    - Blurred vision
    - Mood changes

Ketoacidosis
1 - Common
2 - Rare
G - Rare

Management
1 - insulin replacement for all patients
2 - Insulin replacement for 40% patients
Modified diet and exercise Oral hypoglycaemics
Parenteral hypoglycaemics
G - Diet modification Insulin replacement

Risk factors
1 - Family history Genetics
Geography (increase further away from equator)
Age – first peak 4-7 years, second peak 10- 14 years
2 - Obesity, metabolic syndrome, fat distribution, race, age,
prediabetes, gestational diabetes, sedentary lifestyle
3 - Ethnicity, PCOS, Overweight, Advanced maternal age
>35 years, History of GDM

60
Q

Outline the pathophysiology of Type 1 diabetes.

A

autoimmune pancreatic beta-cell destruction in genetically susceptible individuals.

patients with insulin deficiency are unable to utilise glucose in peripheral muscle and adipose tissues.

stimulates the secretion of counter-regulatory hormones - glucagon, adrenaline, cortisol, and growth hormone.

glucagon, promote gluconeogenesis, glycogenolysis, and ketogenesis in the liver

patients present with hyperglycaemia and anion gap metabolic acidosis.

61
Q

Explain the acute complications that may result from Type 1 diabetes and its treatment.

A

Hypoglycaemia
More insulin than required for amount of plasma glucose.
• Known as insulin shock
• Most prevalent in Type 1 diabetics
Causes: incorrect insulin administration, excessive
exercise, inadequate carbohydrate intake, infection
Treatment: Immediate replacement of glucose

Diabetic ketoacidosis (DKA)
Serious diabetic complication characterised by extreme hyperglycaemia (above 14mmol/L), decrease in blood pH and metabolic acidosis.
• More common in Type 1 diabetics
• Follows stress ; can lead to coma and/or death
Signs and symptoms: hyperglycaemia signs, ketonuria, ‘rotten apple’ breath, tachypnoea, nausea, dehydration
Treatment – insulin therapy, correct dehydration with fluids/electrolytes, treat acidosis with bicarbonate.

62
Q

Identify the various insulin preparations used to treat diabetes.

A 
Short duration (Fast acting)
• To regulate post prandial increase in blood glucose.
• Normally used in conjunction with longer lasting Insulin.

Short duration
• Basal glycaemic control
• Pre-meal dose to regulate post-prandial increase in BGL.

Intermediate duration
• Between meals/overnight
• Slower uptake and longer duration of action
• Twice daily

Long duration
• Prolonged duration of action
• Once daily

63
Q

Explain how diabetes and related pre-diabetic conditions are diagnosed.

A

Fasting blood glucose level of at 7.0+ mmol/L (normal = 6.1mmol/L or below).

An oral glucose tolerance test should be performed, following consumption of a glucose drink, should be 11+ mmol/L (normal = 7.8 or less).

Random blood glucose test 11+ mmol/L. Patients also have the symptom of polyphagia, polydipsia, and polyuria.

A pre-diabetic would have an impaired fasting glucose, but a normal glucose tolerance test.

HbA1c: Long term measure (3 mos) of glycemic
control; normal levels of glucose produce a normal
amount of glycated hemoglobin. As plasma glucose
increases, fraction of glycated hemoglobin increases; in
diabetics typically 6.5% or higher

64
Q

Describe the 3 main symptoms of hyperglycaemia

A

Polyuria - the need to urinate frequently.
Polydipsia - increased thirst & fluid intake.
Polyphagia - increased appetite.

In hyperglycaemia the person develops polyphagia (increased hunger) due to reduced cellular glucose uptake, thereafter energy shortage. The kidneys are unable to reabsorb the large amounts of glucose being filtered back into bloodstream so it is excreted in the urine. The osmotic effects of the high glucose levels cause an increase in the production of urine; this is
known as polyuria. Increased blood osmotic pressure due to hyperglycaemia causes dehydration. This dehydration triggers an increase in thirst known as polydipsia.

65
Q

Discuss importance of diagnosing gestational diabetes.

A

Gestational diabetes occurs when glucose intolerance develops during pregnancy. It is associated with a high risk of maternal complications and fetal death Insulin resistance can occur in the second and third semester and hyerinsulinaemia can increase fetal growth and enlarge organs. Maternal hyperglycaemia leads to an increase in fetal insulin production resulting in hypoglycaemia in the neonate. Screening for diabetes should be done for all pregnant women, not just those with risk factors, so treatment such as metformin and maternal weight control can be instigated to prevent morbidity and fetal mortality. Follow up is important because gestational diabetes can progress to type 2 diabetes.

66
Q

Compare insulin resistance and beta cell destruction.

A

The process of insulin resistance is characterised by failure of the target cells to respond adequately to insulin. As a result, glucose transporter 4 is unable to translocate to the cell membrane to uptake glucose from the blood, therefore hyperglycaemia persists. The pancreas may increase insulin production, but there is still reduced insulin signalling activity. In beta cell destruction there is a progressive decrease in the number of beta cells.

67
Q

Explain the role of insulin and glucagon in regulation of blood glucose levels.

A

Insulin released from beta cells in the islets of Langerhans in the pancreas in response to raised blood glucose levels. Insulin facilitates the removal of glucose from blood, promoting the storage of metabolic fuels. Glucose transporters are recruited from intracellular storage pools and move to the cell membrane facilitating active uptake of glucose into the cell.

Release of glucagon is stimulated in response to hypoglycaemia, high protein meals, exercise and stress. Glucagon mobilises hepatic glycogen and it is released as glucose into the blood to raise blood glucose levels.

68
Q

List several important drugs that may cause hyperglycaemia or hypoglycaemia

A

Important drugs that cause hyperglycemia include glucocorticoids, phenytoin, tricyclic antidepressants and diuretics (loop and thiazide).

Important drugs that cause hypoglycemia are ACE inhibitors, non-selective β-blockers, ethanol, insulins and oral hypoglycaemics, adrenaline and aspirin (in pain relieving doses)

69
Q

Describe a brief summary of available groups of insulin

A
  • Short acting (rapid) Insulin- pre-prandial dose of insulin to regulate spike in blood glucose following meals.
  • Short acting (prolonged) Insulin- pre-prandial dose of insulin to regulate spike in blood glucose following meals and also will continue to provide regulation of basal levels of blood glucose.
  • Intermediate acting Insulin- normally taken twice daily. Regulates blood sugar between meals and overnight. Slower uptake and longer duration of action.
  • Long acting Insulin- taken once daily. Slow uptake and duration of action is approx. 24 hours.
70
Q

Describe pathophysiology Diabetes ketoacidosis (DKA)

A

Risk factors in this case: Exercise, Neglecting Food/Insulin regime. Diabetes ketoacidosis (DKA) is a complication mainly associated with type 1 diabetes.

Although circulating glucose levels are high, the cells are unable to utilise this glucoseeither due to lack of insulin (Type 1) or decreased cellular response to insulin (Type 2).

It usually occurs in DM patients who are undergoing stress such as fighting an infection or undertaking exercise or those who are not administering insulin as prescribed. This results in further increases in metabolic demands. As the cells cannot utilise glucose, they start to metabolise fatty acids in order to produce energy. Ketone bodies are produced as a byproduct of fatty acid metabolism.

As ketone bodies are acidic, their release lowers the pH of the bold, meaning the bloodbecomes acidic also-this is known as metabolic acidosis. This is a serious medical emergency and requires immediate treatment and close monitoring.

71
Q

Discuss why DKA is more likely for Type 1 rather than Type 2 diabetics

A

DKA most commonly presents in undiagnosed type 1
patients. As these patients produce NO insulin, the body is
forced to utilise other metabolic pathways such as fatsketone bodies- acidosis.

Type 2 diabetics usually continue to produce some Insulin
thus reducing the fatty acid metabolism reliance.

72
Q

Explain acute complications associated with type 1 diabetes and its treatment

A

Hypoglycaemia: Abnormally low blood glucose levels; most commonly occurs due to insulin treatment complications.

Collapse and loss of consciousness occurs due to lack of glucose supply to the brain. Symptoms can range from mild dysphoria, to seizures, coma or death.

Treatment aims to increase glucose levels (Carbohydrate intake- fruit juices etc if conscious/ if unconscious- IV Dextrose)

73
Q

Discuss the relationship between myocardial infarction, glycated haemoglobin and blood pressure

A

Glycated haemoglobin reflects the average level of glucose to which thecells have been exposed during their 120 day life. In uncontrolled diabetic patients, glycated haemoglobin level is consistently high.

Diabetes also leads to renal damage, reducing filtration rate which can result in increased blood pressure. The prevalence of coronary heart disease increases with the duration but not the severity of diabetes.

Coronary heart disease is the most common cause of death in individuals with diabetes because of high levels of LDL and triglycerides, low levels of HDL, platelet abnormalities and endothelial cell dysfunction. All these can lead to the development of atherosclerosis and thrombosis and resulting myocardial infarction.

74
Q

Discuss the importance of adhering to treatment plan in diabetic patients

A

.

75
Q

Why is it routine to perform a repeat glucose tolerance test (GTT) at 6 weeks postpartum?

A

Repeat GTT is required at 6 weeks because the blood sugar readings were grossly abnormal and required treatment with insulin. The impaired glucose regulation puts the mother of the child at increased risk of developing type 1 or type 2 diabetes and cardiovascular disease and has implications for future pregnancies

76
Q

Compare and contrast the two methods for assessing blood glucose levels.

A

Diabetics are able to test their own blood glucose using a glucometer. This measures the blood glucose level during a relatively short period of time. Measuring glycated haemoglobin is a good indication of glycaemia over a longer period of time.

77
Q

Discuss the complications of the hyperglycaemia hyperosmolar state and its treatment.

A

Hyperglycaemia hyperosmolar state tends to occur in the elderly when the blood glucose levels are high. Hyperosmolar itself causes dehydration. The person also excretes large volumes of urine, leading to hypovolaemia and hypotension. This can cause drowsiness, stupor, coma and eventually death. Treatment involves administration of fluids, insulin, and electrolytes.

78
Q

Key manifestations of DKA

A

• Hyperglycaemia,
• Hypotension
• Hypokalemica& Hyponatremia
• Dehydration
• Tachycardia (due to Polyuria)
• Tachypnoea- Kussmauls respirations {gasping
breathing body attempts to dispel carbon dioxide which
is building up},
• Increased acidity of blood- Decreased bicarb (utilised
attempting to buffer pH)

79
Q

What are the main goals of therapy for all patients with diabetes in terms of both symptom control and quantitative targets for fasting blood glucose levels and for the hemoglobin A1c?

A

Self-monitoring of blood glucose (SMBG) is the standard method for day-to-day monitoring of diabetes therapy. The premeal target is 90 to 130 mg/dL, and the peak postmeal target is 180 mg/dL or lower.

Hemoglobin A1c should be measured every 3 to 6 months to assess long-term glycemic control. The target value is 7% of total hemoglobin or lower. With both type 1 and type 2 diabetes, the goal of treatment is to reduce long-term complications, including death.

Type 1 diabetes is treated with insulin replacement. Oral antidiabetic agents are ineffective.

Type 2 diabetes is treated with oral antidiabetic drugs or, if needed, with insulin or another injectable drug, but always in conjunction with a program of diet modification and exercise, and only if glycemic control cannot be maintained by diet modification and exercise.

A diagnosis of diabetes is confirmed if hemoglobin A1c is 6.5% or higher, fasting plasma glucose is 126 mg/dL or higher, casual blood glucose is 200 mg/dL or higher, and the patient has the classic signs and symptoms of diabetes (polyuria, polydipsia, and sudden weight loss that
cannot be attributed to other common causes).

80
Q

Identify the brain area associated with anxiety disorder.

A
  • Amygdala responsible for emotional processes and fear response.
  • Sensory stimuli passes along thalamo-cortical route to the cortex for “higher-level” processing; a second route, from the thalamus to amygdala facilitates faster response to danger based on previous learning
  • During stressful event, amygdala co-ordinates with brainstem nucleus (locus ceruleus) to activate physiological changes linked to sympathetic responses
81
Q

What is the definition of obsessive-compulsive disorder (OCD)?

A

Obsessive-compulsive disorder- intrusive thoughts that produce fear or worry (obsessions) and repetitive behaviors (compulsions) aimed at reduction of associated fear.

82
Q

Discuss principle features of an individual who has obsessive-compulsive disorder.

A

Obsessive-compulsive disorder- intrusive thoughts that produce fear or worry (obsessions) and repetitive behaviors (compulsions) aimed at reduction of associated fear.

  • Theorise OCD is caused by chemical imbalance of neurotransmitter serotonin; vital chemical messages are lost (due to serotonin re-uptake) and OCD symptoms develop
  • Cortex becomes hyperactive, sends out equivalents of false alarms; when false signals reach basal ganglia they ‘lock’ into hyperactive transmission of distress signals back and forth to one another. Many view OCD as a “shake in the mind”, similar to tremors seen in Parkinson’s patients (both disorders based on irregularities of neuronal synapse in basal ganglia)
  • A striking link between GAS and OCD. In susceptible children, strep throat can trigger autoimmune response (acute rheumatic fever) that affects the basal ganglia and leads to symptoms of OCD and tic disorders.
83
Q

Describe the causes of PTSD and symptoms.

A
  • Post-traumatic stress disorder
  • symptoms (e.g. disturbing recurrent flashbacks, hyperarousal) that continue for more than a month after the occurrence of a traumatic event.
  • Post-traumatic stress disorder is the only major mental disorder with a known cause (an event that threatens one’s physical integrity or that of others and induces a response of intense fear, helplessness or horror)
  • Theorised that the ventromedial prefrontal cortex fails to inhibit the amygdala, whose hyperactivation leads to an increased fear response, impaired extinction of traumatic memories and deficits in emotion regulation
84
Q

Define diabetes mellitus

A

Dysregulation of blood glucose homeostasis caused by hyposecretion or hypoactivity of insulin.

z Clinical Science (4 decks)

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