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.
