W7 Cardiac Dysfunction Flashcards
Define the following terms: anaemia, polycythaemia, leukopenia, leucocytosis, leukaemia, thrombocytopenia, thrombocytosis and pancytopenia.
anaemia: haemaglobin concerntration ↓ normal
polycythaemia: too ↑ haematocrit.
leukopenia: ↓ WBC count
leucocytosis:
leukaemia: cancer of blood forming tissues
thrombocytopenia: ↓ platelet count
thrombocytosis: ↑ platelet count
pancytopenia: all blood cells ↓ count
Paenia = now
Define haematocrit and outline the normal ranges of blood cell count.
A way of measuring plasma and RBC. A machine shakes the liquid and therefore seperates it.
The plasama component is aqueous solution of NaCL, with ↑ protein contents (albumin, completment, proteins) hormones, chylomicrons, lipoproteins, glucose etc.
Normal WBC count 4-11 x 10 9/L
MALE 40-54%
FEMALE 36-46%
Critical values <15% or >
Define anaemia and describe its clinical manifestations.
Anameia: haemaglobin concerntration ↓ .
Erythrocytes contain hemoglobin protein → carries O2 from the lungs to the rest of tissues.
↓ does not contain enough erythrocytes (RBC)
↓ the erythrocytes do no produce enough haemoglobin.
Molecules contain 4 haemogroups binding sites ++ and attracts - oxygen for transport
Outline the 3 main mechanisms of developing anaemia and exemplify.
- Tissue hypoxia ( lack of oxygen supply) leads to fatigue, weakness, dyspnea and angina.
- Brain hypoxia results in headache and faintness
- Tachycardia and palpitation to ↑ cardiac output.
- Deficient RBC production
- ↓ Hb synthesis = iron deficientcy
- ↓ DNA synthesis = B12 anamia
- ↓ stem cell proliferation = bone marrow depression
- ↓ precursor cell development = ↓ erythropoietin synthesis - ↑ RBC destruction or loss
- Blood loss.
- Acute = child birth, injury surgery
- Chronic = tumours, hemorrage car accident
Explain how anaemia is classified based on RBC characteristics.
RBC indices are apart of complete blood count (CBC) test.
a. Average RBC size (mean corpuscular volume MCV)
b. Haemoglobin amount per RBC (mean corpuscular hemoglobin MCH).
- MCV ↓ than lower limit of normal: microcytic anaemia
2, MCV within normal range: normocytic anaemia - MCV =↑ than upper limit of normal: macrocytic anaemia
- MCH ↓ than lower limit of normal: hypochromic anaemia
- MCH within normal range: normochromic anaemia
- MCH ↑
Describe different types of anaemia
- Iron deficiency anaemia
- ↑ Hgb synthesis
- Microcytic (small erythrocytes), irregular shape and size.
- Hypochromic (pale erythrocytes.
- Blood loss (fecal or menstrual)
- Dietry deficiencyy
- ↑ demand (pregnancy)
- Deficincy in ferrtin (iron stores). - Megalobastic anaemias.
- ↓ DNA synthesis
- - Cobalamin (vit B12) deficiency
- - Folic acid (vit B9) deficiency
- Macrocytic ( erythrocytes are large, but poorly developed)
- Neutrophils are hypersegmented, - Pernicious anaeemia ( ↓ DNA synthesis)
- Causes by a lack of intrinsic factor. (screted from stomach which allows absoprtion of vit B12).
- Slow onset
- Large defective cells die early. - Aplastic anaemia
- Caused by bone marrow depressions - drugs, toxins, radiation, chemotherapy - Chronic disease anaemias:
- Chronic inflammation, chronic renal failure. - SICKLE CELL DISEASE:
Haemolytic anaemia
- Genetic aetiology → mutation in the gene for the hemoglobin beta chain protein.
- Causes an inappropriate hemoglobin accumulation in RBC, leading to an abnormal RBC phenotype → sickle cells.
A. Sickled cells block capillaries:
- Acute pain
- Infarctions cause chronic damage to liver, spleen
- Pulmonary infarcation → acute chest syndrome,
- Cerebral infarction → stroke
Sickled cells are more likely to be destroyed = damaged cells removd early be spleen causing jaundice.
6. Thalassaemia: inherited blood disorder. Fewer circulating RBC ↓ haemoglobin. Manifestations: - fatigue - weakness - facial bone deformities - slow growth Management: blood transfusion, chelation therapy, splenectomy
- Haemolytic disease of newborns: destruction of RBC with release of haemoglobin.
mther is Rh-neg and baby is Rh- positive. Risky for second child.
Define polycythaemia and describe its clinical manifestations.
An abnormal high total RBC mass, hematocrit greater than 50%
- Relative polycythaemia: the haematocrit rises because of a loss of plasma volume without a corresponding ↓ in red blood cells.
- Absolute polycythamia: Th haematocrit ↑ because of an ↑ in total rd blood cells.
Manifstations:
- ↑ blood viscosity and blood pressure
- Splenomegaly (enlargement of spleen)
- ↑ coaguability (blood clotting, thrombosis
Describe the 4 different types of leukaemia
A neoplastic disorder which there is uncontrolled proliferation of leukocytes. Occurs as a malignant neoplasm of heamatopoietic stem cells (in bone marrow).
Creates an abnormal number of immature WBC.
Lymphocytic: over production of lymphoid cell line (B cell and T cell)
Myelogenous/myeloid: overproduction of myeloid cell line (monocytes/ granulocytes.
Risk factors: smoking, benzene exposure, ionising radiation.
- Chronic lymphocytic leukemia: affects lymphoid cells and grows slowly. >55 years old.
- Chronic myeloid leukemia: affects myeloid cells
in acute leukemia WBC completely loss functionality - Acute lymphocytic leukemia: affects lymphoid cells and grows quickly. Most common in adults.
- Acute myeloid leukemia: affects myeloid cells and grows quickly.
Define coagulopathy and outline the two main types.
When hemostasis goes wrong.
1. Hypercoaguability - ↑ coagulation of the blood: Predisposes to thrombosis (clot formation within undanaged blood vessels) and embolus ( clot travlling through the circulatory system).
- Bleeding disorders - ↓ coagulation of the blood: Platelet disorders
- THrombocytopenia - ↑ platelet numver
- THrombocyopathia - ↓ platelet function.
Genetic coagulation disorder, acquired coagulation disorders
Describe the causes and clinical manifestations of hypercoagulation.
Mainly causes by
- ↑ platelet number
- Endothlial damage
- ↑ pro-coagulation factors
- ↓ anti-coagulation
Manifestations:
1. Heart or lungs: vest pain, shortness of breath, upp body discomfort.
2. Deep veins of the lower limbs: pain, redness, warmth and swelling in the lower limb.
3. Brain: headaches, speech changes, dizziness, and trouble speak - which suggest stroke
Describe the mechanism of action of drug groups used to control hypercoagulability.
Preventing fibrin deposits, no direct effect on a formed clot
1. Anticoagulant drugs:
Heparin: inactivates coagulation factors
Warfrin: inhibits vitamin K →↓ the synthesis of coagulation factors
2. Antiplatelet drugs:
Aspirn, clopidogrel: prevents platelet aggregation
Dissolving clots
3. Thrombolytic/fibrinolytic drugs:
Streotokinase: converting plasminogen → plasmin, which digests fibrin clots
Define and explain the pathogenesis of disseminated intravascular coagulation.
It is a throbohaemorrphagic disorder usually associated with a serious illness. Manifests as widespread formation of clots throughout the vasculature which cause vessel occlusion and tissue ischemia (limited blood flow to tissue) .
All available coagulation proteins and platelets are consumed and severe haemorrhage results
Explain how thrombocytopenia may develop and its clinical manifestations.
Decreased platelet levels (thrombocytopania).
- ↓ production
- ↑ destruction
- Platlts usd up in forming clots.
Symptoms
- Abnormal colour on urine
- Abnormal (heavy or prolonged) menstrual periods
- Abnormal vaginal bleeding
- Bleeding under the skin in tissues- GIT bleeding
- Vomiting blood
- Nosebleeds.
Causes: Haemophilia ( genetic; lack of coagulation factors, vitamin K deficiency
Explain how thrombocytopenia is treated.
- Vitamin K supplementation
- Synthetic coagulation factors
- Antifibrinolytic agents
Define hypertension.
Sustained elevation of systemic arterial blood pressure. It creates excess pressure on arterial walls, which damages the endothelium over time.
On measurement
→ Diastolic pressure of 90mmHg or ↑
→ Systolic pressure of 140mmHg or ↑. Needs to be determined over a period of time
Cite and explain the two major determinants of hypertension.
- Peripheral resistance: the narrower the blood vessels, ↑ pressure of blood against vessel walls
- Many factors can cause vasoconstriction
- Blood vessles may b damaged and lose elasticity. - Volume of blood circulating: the ↑ the volume, ↑ the pressure of blood against vessel walls.
- stroke volume may in ↑ if the body is retaining fluid.
- A chronic ↑ in HR will ↑ the amount of blood pushed around the body per minute (cardiac output).
Describe primary hypertension and the range of factors that may contribute to it.
Primary hypertention is a complex multifactorial condition. Contributing factors: - age, gender, family history - diabetes mellitus - lifestyle factors: - increased stress - high salt intake - lack of PA - obesity x Overactive SNS xOveraction renin-angiotension-aldosterone system (↑ BP, rentention of salt and water) xLow responsivness of natriuretic pepetides BP ↓ x Metabolic
Define secondary hypertension and exemplify with possible aetiologies.
Secondary hypertension reder to when a case is evident: ↑ in cardiac output, total peripheral resistance.
- Renal hypertension: disorder of renal blood flow and RAAS
- Disordersof adrenocorticosteriod hormones
Explain how hypertension can cause target organ damage.
Heart: - Left ventricular hyprtrophy - Angina or prior myocardial infarction - Prior coronary revascularisation - Heart failure. Brain: stroke or transient ischemic attach - Chronic kidney disease - Peripheral arterial disease - Retinopath - Erectile dysfunction
Describe the major anti-hypertensive drug groups, their mechanisms of action and use.
DIRECT REDUCTION OF BLOOD PRSSUR → FAST
1. Drugs that directly reduce vascular resistance → increase peripheral vasodilation.
INDIRECT REDUCTION OF BP → LONG-TERM
2. Drugs that reduce stroke volume - the volume of blood pumped from the left ventricle per beat, (diuretics, ↓ RAAS)
3. Drugs that reduce HR, thus reducing cardiac output (calcium channel blockers)
4. Drugs that reduce activation of sympathetic pathways → thus deducing vasoconstrition.
Outline modifiable lifestyle risk factors in Hypertension.
PIC 19
Define arteriosclerosis and atherosclerosis and describe their aetiology.
ARTERIOSCLEROSIS: Slowly progressive disease caused by endothelial damage and adaptation. Modifying the characteristics of arterial walls.
Risk factors
- smoking
- hypertention, heart disease
- ↓ levels of cholesterol and LDLs
- unmanaged diabetes mellitus, obesity
- old age, ↑ PA.
MANIFESTATIONS:
- Thickening
- Loss of elasticity (stiffening)
- Plaque build up (atheroslerosis)
- Calcification
ATHEROSCLEROSIS: Deposition of fat in the walls of the arteries → formation of plaques. → leads ti degenerative changes in arteries which affect elasticity and become narrower.
Risk factors: High fat diet - high blood cholesterol levels - high triglycerids - inadquatee levels of one for more fats - obesity - High BP - Diabetes - Heavy alcohol use - smoking
Discuss the roles of lipoproteins in atherosclerosis.
The more protein, the ↑ the density.
The more lipid, the ↓ the density.
Dietry lipids are absorpd as chylomicrons → adipose and muscle cells take up lipids from chylomicrons →chylomicron remnants are intermediate-density lipoproteins (IDL) → IDS become low- density lipoproteins (LDL - bad cholesterol), delivering fat to other tissues.
High-density lipoproteins (HDL good cholesterol) are made in the liver
Describe the pathogenesis of atherosclerosis.
Atherosclerosis → ndothlial damage + excssie fats.
It developes because scavenger WBC encounter the fatty deposits in the artery lining and try to destory the fats by oxidising them.
- Oxidizd fats injure the endothelium
- Clots form and growth factors are released
- Smooth muscle grow over the fatty core.
1. After an endothelial injury, vascular permeability increases 2. LDL molecules enter the vascular endothelium and are oxidised 3. Monocytes differentiate into macrophages and phagocytose LDL foam cells 4. Foam cells release cytokines and growth factors (chronic inflammatory response) that promote plaque formation 5. Endothelial cells covers the plaque 6. Plaque accumulates calcium salts over time and hardens 7. Plaques narrow or block arteries, causing ischemia (decreased blood supply to a body organ or part)
Distinguish between stable and unstable plaques formed in atherosclerosis.
Stable plaque: have thick fibrous caps. They ↓ blood flow by partially blocking vessles, but do not rupture to form clots,
Unstable plaques: have thin fibrous caps. These plaque can rupture and cause a clot to form. Thy may completely block the artery , clot may break free and become an embolus
Outline the possible consequences of atherosclerosis.
- Coronary heart disease
- Stroke
- Peripheral Artery Disease
- Arterial aneurysms
Explain how atherosclerosis causes coronary heart disease and further progresses.
If atherosclerosis block the coronary arteries the resulting ischemia may cause:
- Angina
- Myocardial Infarction
- Cardiac arrhythmias
- Conduction deficits
- heart failure
- sudden death
Define angina and compare the different types and clinical manifestations.
Angina pctoris: pain due to a myocardial ischemia ( ↓ blood flow) → may be accompanied by referred pain in the arms shoulders and neck.
Stable angina: pain when heart oxygen demand ↑
Unstable angina: pain at random times, could be a symptom of acute myocardial necrosis
Prinzmetal (variant) angina: pain when coronary arties spasm
Silent myocardial ischemia: myocardial ischemia without pain
Describe the mechanisms of action of pharmacological drugs used to treat angina.
Pharmacological management of angina aims to reduce ischemia by either:
- Restoring blood flow by relaxing coronary artery smooth muscle (to dilate the coronary arteries and ↑ perfusion).
- Vasodilator drugs such as calcium channel blockers, verapamil, diliazem, organic nitratse. - Reducing the metabolic deman of the heart by reducing heart rate and contractility. - beta-adrenoceptor antagonists (beta blockrs).
Define chronic ischaemic heart disease and explain its development and management.
Chronic Iscemic heart disease: imbalance in blood supply and the hearts demands for oxygen. REDUCED BLOOD SUPPLY REUSLTS FROM - Atherosclerosis - Vasospasm - Thrombosis HIGHER OXYGEN DEMANDS (stable angina) - Mental Stress - Exercise - Ecxposure to cold MANAGEMENT: - Life style changes - Hypertension management - Lipid-lowering therapy (statins) - Nitroglycerins ( vasodilation
Explain the mechanism of action of statins.
Decrease synthesis of cholesterol → inhibition of HMG-CoA enzyme,
↑ uptake of LDL by the liver (remove it from blood) → ↑ number of LDL receptors
Describe the types of acute coronary syndromes and their correlation with angina.
Acute coronary Syndromes (ACS) is the rupture of atherosclerotic plaque leading to thrombosis and disrupts blood flow.
Non-ST-segment eelevation → acute coronary syndrome = unstable angina.
↓
Myocardial necrosis:
- Non-ST-segment elevation myocardial necrosis.
- ST-segment elevation myocardial necrosis
Define acute myocardial infarction and its clinical manifestations.
Acute Myocardial Infarction (AMI): necrosis in myocardium due to obstructed blood flow for more than 20 min.
Chest pain: severe, crushing, constrictive, or like heart burn.
Sympathetic NS response
- GI distress, nausea, vomiting, dyspnoea
- Tachycardia and vasoonstriction
- Anxiety, restlessness, feeling of impeeding doom,
Hypotension and shock
- Weakness in arms, les, syncope or presyncope episode.
Correlate levels of coronary obstruction with the extent of myocardial injury.
PIC
Explain how the extent of myocardial injury can be diagnoses based on an ECG.
PIC
Non-STEMI is produced by partial obstruction of coronary artery: → superficial myocardial tissue is still able to get oxygen → ECG shows an ST depression or T inversion → abnormal electrical conduction
STEMI → indicates ischemia of the whol myocardial layer irrigated underneath that point → an ST elevation indication imparted electrical conduction during ventricular systole. .
- More precise definition of heart attack due to ↑ risk sudden death. Prevention of death requires rapid recognition, O2 reperfusion tx and management
Describe the medical interventions used to manage acute myocardial infarction.
Pharmacological: - Supplemental oxygen - Short acting subligual nitroglycerin - Antiplatelet therapy (asprin) and anticoagulation (heparin) therapy - Intravenous nitroglycerin - Morphine sulphate to manage pain - High- intensity therpy - Oral beta blockers. INVASIVE STRATEGIES - Percutaneous coronary intervention in STEMI - May be performed in non-STEMI - Coronary Arterial Bypass graft
Describe the body responses following myocardial infarction.
After myocardial infarction: ncrotic areas undergo inflammatory processes (7 days). 1-3 → inflammation recedes. Resolved adter 4 weeks → replaced by fibrous tissue.
Remodeling induced by:
- Inflammatory mediators released after necrosis.
- Hormones released during sympathetic NS activation. + hormones.
List and describe the types of cardiomyopathies and their possible aetiologies.
Possible aetiologies:
- Dilated: ventricles are too weak to pump blood out.
- Hypertrophic: overworked ventricles get unusually thich tso they are unable to relax and fill up blood in diastole (due to hypertension)
- Restrictive: ventricles are to still to stretch or obstructed with scar, fibrous tissue, tumour.
Congenital: defects in their contractile protein make cells too weak.
Secondary hypertension: the chronically increased peripheral resistance overloads the heart
Describe abnormalities of cardiac valves and how that affects the cardiac cycle
The endocardial structurs lining the heart can cause heart failure.
- If the AV valves leading into the ventricles do not work
- If the semilunar valves leading out of the ventricles do not work.
HEART MURMURS: If a valve is stenotic you hear blood shooting through the narrow opening when the valve is open
If a valve is regurgitant, you hear a murmur of blood leaking back through when the valve should be closed. LUB DUB.
Explain how heart failure can develop from hypertension, atherosclerosis and AMI.
Heart failure eis a condition that develops when the heeart cannot pump nough blood to meet the bodies needs. In some cases the heart can’t fill with enough blood/ cant pump blood to the rest of the body with enough force.
Describe and compare systolic and diastolic heart failures.
Systolic failure: heart fails to contract.
- Dilated heart → decreased contractility → blood pooling in the heart
- Impaired ejction of blood from the heart during systole
- ↓ ejection fraction: no
Diastolic failur: heart fails to relax:
- hypretrophic hart → dcreasd ventricular compliance → heart cannot fill up propery
Discuss the pharmacological agents used to treat systolic and diastolic heart failure.
- Increase contractility (in systolic heart failure)
- Cardiac glycosides
x ↑ contratile force
x ↓ conduction throuh AV node
x ↓ HR - ↓ afterload
- ACE inhibitors
- Diuretics - Decrease HR; beta-blockers
( REDUCING STRAIN ON THE HEART BY REDUCING BLOOD PRESSURE AND HR)
Distinguish between the systemic effects of left and right-sided heart failure
LHS HEART FAILURE
Leads to pulmonary congestion → progresses ro RS failure.
Systolic: LV does no pum enough blood to body.
Diastolic: LV does not accept enough blood from lungs
RHS HEART FAILURE:
Leads to peripheral congstion → progresses to LS failure
Systolic: RV does not pump enough blood to lungs
Diastolic: RV does not accept enough blood from body
Discuss the progression of the major cardiovascular disorders.
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Define dysrhythmia and describe how it may follow myocardial ischemia and infarction
“Dysrhythmia”
Abnormality automaticity → congenial, psychogenic, ANS.- Bradycardia: HR <60 bpm
- Tachycardia: HR >100bpm
Abnormality in conductivity → usual a sequelae of MI.
- Heart block in AV nod
- Ectopic pacemaker
- Premature ventricular contraction (PVC).
Atrial flutter
Atrial fibrillation
Ventricular fibrillation
Conduction blocks: when they myocardium damaged by necrosis, cannot conduct electrical signal = dysrhythmia.
Describe the mechanism of action of anti-dysrhythmic drugs
Cl ass I: Block sodium channels ↓ cardiac AP.
Class Ia: quinidine
Class Ib: lignocaine
Class Ic: flecainide
Class II: beta-blockers - ↓ AV conduction and contractility.
Class III: ↑ the duration of AP and affect refractonary period.
Class IV: block calcium channel
Define shock, outlining the 5 types and clinical manifestations.
Circulatory shock reeprents the inability of the circulation to adequately perfuse the tissues of the body
Describe the aetiology of the five types of shock
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Explain how shock may progress to multiple organ dysfunction syndrome.
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Discuss the medical interventions performed in shock.
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