PATH written test (weeks 7-12)

stable angina

Atherosclerosis (narrowing of the coronary arteries due to plaque buildup) occurs. The person will have stable plaque. When the person is at rest the heart does not need as much blood supplied through the coronary arteries, but when the heart is exerted (e.g physical movement) the heart rate quickens and the demand for blood supply through the coronary arteries increases. Because of the atherosclerosis the increased demand cannot be met, which causes anaerobic metabolism to occur, causing lactic acid and hydrogen buildup which then causes angina. The angina is relieved with rest as the blood demand goes back down and the coronary arteries are able to supply enough blood again. The angina can also be relieved with nitrates which are vasodilators.

categories and subcategories of coronary artery disease (CAD)

ischaemic heart disease & acute coronary syndrome

ischaemic heart disease: stable angina, vasospastic (prinzmetal) angina, & silent myocardial ischaemia

acute coronary syndrome: unstable angina, STEMI, NSTEMI

vasospastic (prinzmetal) angina

A decrease in supply of blood to the heart muscle because of vasospasm. A dysregulation of vasoactive substances causes vasospasm or constriction of the coronary arteries, leading to pain.

silent myocardial ischemia

Symptoms with no pain

Common in diabetic patients who aren't controlling their blood glucose, which leads to damage to their blood vessels. Nerves need blood flow, so if the blood vessels that go into those nerves are damaged, then those nerves can be damaged as well. so this person will get myocardial ischaemia because of the decrease in blood flow to the heart, but they won't get the typical heart pain sensation because of the nerve damage.

Symptoms associated with right heart failure and pathophysiology:

The right side of the heart pumps blood from the body (systemic circulation) to the lungs (pulmonary circulation). Insufficient cardiac output from the right ventricle will cause blood to backlog into the right atria, vena cava, and the systemic circulation (rest of the body). Patients may present with jugular vein distension, ascites (abdominal oedema) and peripheral oedema. The most common cause of RHF is LHF. This is due to the increase in pulmonary blood vessel pressure from the backlog of blood caused by LHF. This increases right ventricular afterload (the resistance that the ventricle needs to overcome to eject blood out), which means that the right ventricle needs to work harder. This eventually reduces ventricular compliance (the ability of the ventricles to stretch), which decreases preload and stroke volume.

Symptoms associated with left heart failure and pathophysiology:

The left side of the heart pumps blood from the lungs (pulmonary circulation) to the body (systemic circulation). If the cardiac output of the left ventricle is ineffective to pump blood into the systemic circulation, blood backlogs into the Left Atrium, and then into the pulmonary circulation (lungs). When the pressure increases in the pulmonary circulation, fluid begins to shift out of the intravascular space, and into the interstitial space of the lung (alveoli). This results in fluid accumulation in the lung (cardiogenic pulmonary oedema), impairing ventilation. The two most common causes of LHF are hypertension and myocardial infarction. Hypertension causes the left ventricle to work hard to overcome the increase in afterload. This causes dysfunctional hypertrophy and a decrease in compliance resulting in a decrease in preload and Stroke Volume. A Myocardial Infarction that affects the left ventricle will mean that the infarcted part of the myocardium will not work properly.

Cor pulmonale

right sided heart failure due to chronic pulmonary hypertension. Decreased ventilation of alveoli can cause hypoxia. To prevent a V/Q (ventilation / perfusion) mismatch the body causes vasoconstriction of the blood vessels around that area. If this is widespread, then this increases resistance to blood flow. This causes pulmonary hypertension and increases the afterload of the right side of the heart. The right side of the heart has to work harder to overcome this resistance. Over time, the right ventricle undergoes hypertrophy, which leaves less space inside the chamber to fill with blood, thereby decreasing preload. This is known as diastolic heart failure.

Insufficient cardiac output from the right ventricle will cause blood to backlog into the right atria, vena cava, and the systemic circulation (rest of the body). Patients may present with jugular vein distension, ascites (abdominal oedema) and peripheral oedema.

Cardiogenic pulmonary oedema

a build up of fluid (oedema) in the alveoli of the lungs due to a dysfunction of the left side of the heart (left heart failure). The left side of the heart takes blood from the lungs (pulmonary circulation) and pumps it to the rest of the body (systemic circulation). If the left side of the heart fails then the pressure builds up in the pulmonary circulation. This could be due to systolic dysfunction of the left side of the heart (eg from a myocardial infarction) or due to diastolic dysfunction (eg cardiac hypertrophy due to chronic hypertension.

The mitral valve connects the left atrium and the left ventricle. The aortic valve separates the left ventricle and the aorta. If there is regurgitation, the valves don't close properly, and blood is allowed to flow backwards. If there is stenosis the valves don't open fully and less blood is able to leave the left side of the heart. Both of these situations could cause back log of blood in the pulmonary circulation.

Increased hydrostatic pressure in the pulmonary circulation leads to fluid entering the alveoli this pulmonary oedema will decrease ventilation and make it harder for gasses to diffuse in and out of the alveoli. Acute treatment includes PEEP (positive end-expiratory pressure) to increase the pressure in the alveoli and vasodilators to decrease the hydrostatic pressure inside the capillaries surrounding the alveoli.

H's & T's of Cardiac Arrest - reversible causes

Hypoxia, Hypovolaemia, Hypothermia, Hyper/hypokalaemia, Hydrogen ion excess, Tension pneumothorax, Tamponade, Toxins, Thrombus.

Diabetes Mellitus vs Diabetes Insipidus

Type 1 Diabetes Mellitus (DM)

Cause: Genetic predisposition + trigger (infection, stress, trauma) → autoimmune destruction of pancreatic β-cells → no insulin production.

Onset: Usually childhood/adolescence.

Insulin: Always required.

Symptoms: 3 Ps: Polyuria – excess urination, Polydipsia – excess thirst, Polyphagia – excess hunger (cells starved of glucose)

Weight loss, fatigue, risk of diabetic ketoacidosis (DKA).

 

Type 2 Diabetes Mellitus (DM)

Cause: Lifestyle and genetic factors → insulin resistance + eventual β-cell dysfunction.

Onset: Usually adults, often linked to obesity and sedentary lifestyle.

Insulin: Sometimes needed later, but not always initially.

Symptoms: 3 Ps (polyuria, polydipsia, polyphagia)

Often gradual onset, may go undetected for years.

Long-term complications (neuropathy, nephropathy, cardiovascular disease).

 

Diabetes Insipidus (DI)

Cause: Problem with ADH (antidiuretic hormone/vasopressin):

Central DI – insufficient ADH production.

Nephrogenic DI – kidneys fail to respond to ADH.

Onset: Any age.

Insulin: Not involved (unrelated to glucose).

Symptoms: Polyuria – very large volumes of dilute urine, Polydipsia – intense thirst.

NO polyphagia (glucose metabolism is normal).

Risk of dehydration and electrolyte imbalance.

Diabetic Ketoacidosis

Type 1 diabetes:

-A person is born with a genetic susceptibility to type 1 diabetes

-They undergo a triggering event (eg. infection)

-An autoimmune response causes the destruction of beta cells of the islets of Langerhan in the pancreas

-Therefore they now lack the ability to create insulin (type 1 diabetes)

 

Diabetic ketoacidosis:

-If there is a lack of insulin, glucose can not enter the cell

-Gluconeogenesis is stimulated, which is the creation of glucose from non carbohydrate sources

-Glycogenolysis (breakdown of glycogen (stored glucose) also occurs)

-This increases blood glucose / hyperglycaemia

-The breakdown of fat occurs (lipolysis)

-However, fat burns in a carbohydrate flame so incomplete catabolism of fat occurs due to no glucose being able to enter the cell.

-Therefore ketones are produced

-Ketones are acidic therefore, metabolic acidosis occurs

HHS - hyperosmotic hyperglycaemic state

 A patient with Type 2 diabetes mellitus has insulin resistance and/or reduced insulin production. They experience a triggering event (eg. infection, MI, illness). This increases stress hormones (glucagon, cortisol, epinephrine), which increases insulin demand. There is a relative insulin deficiency due to insulin resistance and/or impaired insulin secretion. Some insulin is present, but not enough to control blood glucose. Some insulin allows limited glucose uptake into cells, so cells are not completely starved of energy (unlike DKA). However, excess glucose remains in the blood → severe hyperglycaemia. Gluconeogenesis is stimulated because there is a relative insulin deficiency, so glucose uptake into cells is reduced. The cells perceive a state of relative starvation (even though blood glucose is high). This triggers the release of counter-regulatory hormones (glucagon, cortisol, epinephrine), which stimulate the liver to increase gluconeogenesis and Glycogenolysis. This further increases blood glucose levels.

 

When blood glucose is very high, glucose spills into urine (glucosuria). This causes osmotic diuresis which leads to large fluid loss (polyuria). This results in severe dehydration and increased serum osmolarity (hyperosmolar state). Water shifts out of cells (including brain cells), leading to neurological symptoms (confusion, seizures, coma). Some insulin is still present, therefore lipolysis is reduced (but not completely absent). Insulin inhibits the breakdown of fat, so there is no significant ketone production since fat requires carbohydrate for complete metabolism (“fat burns in a carbohydrate flame”). Since some glucose can still enter cells, there is enough carbohydrate available to generate pyruvate. Pyruvate is converted to oxaloacetate, which allows the Krebs cycle to function normally. This means acetyl-CoA from fat metabolism can enter the Krebs cycle instead of being converted into ketones. Therefore ketone production is prevented and no metabolic acidosis occurs (unlike DKA)