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Jorge's CAR > Week 7 > Flashcards

Week 7 Flashcards

1
Q

Neutrophil Histology

A

lobulated nucleus (2-4 lobes)
pale pink or light blue cytoplasm
Band neutrophils are young neutrophils - nucleus lacks segmentation

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2
Q

Basophil and Eosinophil histology

A

Difficult to differentiate
Lobulated nucleus
Basophils : dense blue granules
Eosinophils: orange-red granules

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3
Q

Monocyte histology

A

irregular shaped nucleus
blue-grey cytoplasm

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4
Q

Lymphocyte histology

A

nucleus round with condensed chromatin
pale blue cytoplasm

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5
Q

Mammalian Erythrocyte Differentiation

A

Dog: more concave than cats, white center
Cat: smaller than dogs, uniform colour
Horse: coagulates
Ruminants: crenation (spikes)
Avian and reptile: elliptical and nucleated

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6
Q

Immunological basis of blood groups

A

Determined by presence of antigens on surface of erythrocytes

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7
Q

Alloantibodies =

A

specific antibodies directed against erythrocyte antigens present in the same species
Important in determining blood transfusion success
May cause agglutination and/or haemolysis

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8
Q

Dog blood typing

A

DEA = dog erythrocyte antigen
DEA1.1 (most immunogenic - no naturally occuring antibodies)
DEA 1.2 (no naturally occuring antibodies)
DEA 1.3
DEA 3, 4, 5, 6, 7, 8
DAL - dalmations

Dogs can only be +ve for 1 of DEA1.1, 1.2 and 1.3 (or null type)

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9
Q

Cat blood typing and transfusion

A

A, B and AB
Highly immunogenic
Type A - low level of anti-B alloantibody
Type B - high level of anti-A alloantibody
Type AB - no alloantibodies

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10
Q

Horse blood typing and clinical relevance

A

7 blood groups (A, C, D, K, P, Q, U)
Mares pregnant with foal of different blood type can become sensitised to foals blood and produce alloantibodies which are ingested in colostrum and attack RBCs of future foals of the same blood type = neonatal isoerythrolysis

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11
Q

Blood group testing

A

Snap tests:
Tests for DEA1.1 and 1.2 in dogs
Tests for A,B and AB in cats
Blood typing cards:
only for dogs
antibodies embedded in paper cause agglutination

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12
Q

Assessing blood compatability

A

Blood cross matching:
Major cross match detects if recipients serum contains antibodies against donor RBCs
Minor cross match does the opposite

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13
Q

Erythrocytes adaptations

A

Biconcave disc increases surface area
Elasticity for travel through capillaries
Energy from anaerobic metabolism of glucose so don’t use up oxygen
No nucleus increases room for haemoglobin

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14
Q

Origins of erythrocytes

A

Eryhthropoeisis occurs in red bone marrow and spleen
Formed from stem cells
Require adequate amounts of: protein, iron, copper, folic acid and vitamins

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15
Q

Source and effect of erythropoeitin

A

= hormone that regulate RBC production
Embryonic life source: yolk sac, liver, kidney, spleen, bone marrow
Adult life source: kidney
Effect:
Decreased O2 transport -> erythropoeitin secretion from kidneys -> travel to bone marrow -> EPO binds to receptors on erythroid cell precursors -> increased RBC production

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16
Q

Removal and breakdown of RBCs

A

As RBCs age they lose sialic acid residues from the surface -> exposed galactose moieties which induces phagocytosis
They become more fragile and swell due to failure of normal membrane function
Haem is recycled, iron is recycled and stored in liver, amino acids are reabsorbed and bilirubin is excreted in bile

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17
Q

Iron metabolism

A

Free iron is toxic
Iron molecules released from haem are conveyed into bone marrow by transferrins or stored as insoluble iron in macrophages and hepatocytes (liver cells) as ferritin

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18
Q

Lab blood tests

A

Haemocytometer - RBC cell
Microhaematocrit - PCV
Microscopic exam of blood smears
Automated analysers

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19
Q

Microhaematocrit

A

measures PCV = ratio of blood volume occupied by RBCs to the volume of the whole blood

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20
Q
A
21
Q

Haematology analysis/automated cell counters and limitations

A

Coulter principle - enumerate and identify blood cell populations
Streams of cells pass through an aperture with an electrical current flowing across it
Passing cells disrupt electrical current creating a pulse
Frequency of pulses = number of cells
Amplitude = cell volume
Absorbance measure haemoglobin

Limitations:
don’t give reliable cell count
small RBCs can be counted as platelets
large platelets can be counted as RBCs

22
Q

PCV, MCV, MCH, MCHC

A

PCV = packed cell volume - fraction of whole blood occupied by RBCs - = MCV x RBC count / 100

MCV = mean corpuscular volume - average vol of RBCs

MCH = mean corpuscular haemoglobin - average amount of Hb per RBC (pg) - = Hb x 10 / RBC count

MCHC = mean corpuscular haemoglobin concentration - average conc of Hb in cell relative to size/volume (g/dl) - = Hb x 11/Hct

23
Q

Anemia causes and characteristics

A

= capacity of blood to transport oxygen reduced
Reduced RBC number
Reduced Hb per RBC

Cell size:
Macrocytic
Normocytic
Microcytic

Hb content:
Hypochromic
Normochromic
Hyperchromic

Reticulocyte count:
Regenerative (high)
Non-regenerative

24
Q

Ion channels that govern VSM tone

A

Ca channels - mediate contraction/dilation
K channels - mediate hyperpolarisation
Na/K ATPase - provides energy

25
Q

Local mechanisms that regulate arteries and veins

A

Cross-sectional area alters blood flow

Low oxygen -> metabolite build up which are cleared due to reactive hyperaemia

Chronic hypoxia -> angiogenesis

26
Q

Endothelial derived factors that influence vasomotor tone and their cell signalling mechanisms

A

Vasodilators:
Nitric oxide
NO diffused into VSMC and activated guanylate cyclase -> increased cGMP -> vasodilation

Endothelium-derived hyperpolarising factor (EDHF)
Hyperpolarise VSMCs -> reduced contractility

Prostaglandins
Bind to VSMCs and increase cAMP levels

Vasoconstrictors:
Angiotensin II
Bind to VSMCs -> increased Ca levels

Endothelins
Peptide that acts on VSMCs -> increased Ca levels

27
Q

How do hyprophobic signalling factors act within the nucleus

A

Lipid soluble so pass through membrane
Bind to cytosolic proteins e.g. heat shock proteins to form complexes which move into nucleus and release signalling molecule to cause transcription
e.g. hormones

28
Q

3 main classes of cell surface receptor

A

Ion channel (ligand gated) e.g. neurons
G-protein linked e.g. epinephrine receptor
Enzyme linked e.g. insulin receptor

28
Q

3 main classes of cell surface receptor

A

Ion channel (ligand gated) e.g. neurons
G-protein linked e.g. epinephrine receptor
Enzyme linked e.g. insulin receptor

29
Q

Platelet structure

A

Small
Unnucleated
Stored in spleen

Membrane-bound fragments of cytoplasm from megakaryocytes

Surface glycoproteins
Phosphatidyl serine
Rich in microfilaments and microtubules – allow contraction

Organelles -
Alpha granules:
Growth factors
Von Willebrand factor
Coagulation factor 4

Dense/delta granules:
ADP
calcium

30
Q

Haemostasis

A

PRIMARY HAEMOSTASIS
Vascular constriction:
Smooth muscles in wall of injured blood vessel reduce blood flow to site

Platelet plug formation:
Platelet adhesion:
Von Willebrand factor (VWF) released from damaged endothelial cells and alpha granules bind to platelets to promote platelet adhesion

Platelet activation:
Platelets are activated, release ADP, serotonin, platelet activating factor + thromboxane A2
Leads to platelet aggregation with platelets binding to each other through glycoprotein IIb & IIIa (receptors on platelets)
Platelet aggregation
Fibronogen binds glycoproteins IIb/IIIa on adjacent platelets
Enhanced by generation of thrombin

SECONDARY HAEMOSTASIS
Coagulation cascade:
Intrinsic pathway:
Intiated when blood comes into contact with exposed collagen at site of injury
Activation of clotting factors leads to formation of Factor Xa (active form of factor X)

Extrinsic pathway:
Initiated by tissue factor released released from damaged tissues
Converts factor X to factor Xa (presence of Ca ions)

Common pathway:
Factor Xa and factor V form prothrombinase complex
Prothrombinase complex converts prothrombin into thrombin
Thrombin seperates fibrinogen into fibrin which forma meshwork that stabilised the plateley plug, creating a stable fibrin clot

TERTIARY HAEMOSTASIS
Fibrinolysis
Removal of the fibrin clot
Tissue plasminogen activator activated plasminogen to form plasmin
Plasmin breaks down fibrin molecules to remove the clot

31
Q

Thrombocytopenia
Thrombocyopathy

A

= low platelet count
= abnormal platelet function

32
Q

Buccal musosal bleeding time

A

Time taken to stop bleeding after a small incision made
Healthy dog: 1.7 - 4.2 mins
Healthy cat: 1.0 - 2.4 mins

33
Q

Platelet counting methods

A

Haemocytometer
Automated cell count
Blood smear

34
Q

Common causes of heart failure

A

Coronary artery disease
High blood pressure
Cardiomyopathy
Heart valve disorders
Arrythmias

35
Q

concentric and eccentric cardiac hypertrophy

A

Concentric cardiac hypertrophy:
Response to overload on heart due to high BP or narrowing aortic valve
Increased resistance -> thickened ventricular muscle walls to allow heart to generate high pressure to overcome resistance
smaller ventricular chambers -> reduced ability to fill -> diastolic dysfunction (impaired filling)

Eccentric cardiac hypertrophy:
Occurs in response to volume overload on heart due to leaky or dilated valves
Heart muscle responds by stretching and enlarging to accommodate increased blood volume
Dilated heart chamber allows heart to maintain SV and compensate for increased volume
Increased wall stress and dilation -> systolic dysfunction (impaired contraction) and reduced pumping efficiency

36
Q

Pathophysiological responses of cardiac arrest

A

Activation on SNS:
Release of adrenaline to increase HR, constrict blood vessels and increase contractability
Initially helps maintain CO but contributes to heart muscle damage

Activation of renin angiotensin aldosterone system (RAAS):
Kidneys release renin in response to reduced blood flow and pressure
Leads to formation of angiotensin II which causes vasoconstriction, fluid retention + stimulates release of aldosterone
Aldosterone promotes sodium and water retention
Increases blood volume + peripheral resistance
Can worsen heart failure symptoms

Ventricular remodeling:
Includes hypertrophy and dilation of heart failure
Adaptations intially help compensate for reduced pumping ability
Over time impair contractability and distrupt normal heart architecture

Fluid retention:
As CO decreases there is fluid retention in various parts of body
Leads to oedema in lungs, legs and ankles

37
Q

Clinical signs of heart failure

A

Dyspnoea
Weakness
Oedema
Irregular heart beat

38
Q

Mechanisms of how oedema develops

A

Increased capillary hydrostatic pressure:
Reduced CO leads to increased BP
Forces fluid out of capillaries into interstitial spaces

Sodium and water retention:
RAAS activated in response to reduced CO
Results in water and sodium retention in kidney leading to expansion of circulating blood volume

Reduced capillary oncotic pressure:
Reduced production of albumin
-> reduced osmotic force that draws fluid into capillaries
Thus favouring movement of fluid into interstitial spaces

Lymphatic dysfucntion:
Lymphatic vessels become overwhelmed by increased fluid accumulation

Inflammation and endothelial dysfunction:
Disrupted integrity + permeability of capillar walls allows leakage of fluid into interstitial spaces

39
Q

physiological mechanisms by which heart failure can be managed

A

Lifestyle modification: weight management, sodium restriction, fluid restriction

Medications: diuretics, beta-blockers, angiotensin-converting enzyme, aldosterone antagonists

40
Q

Blood pressure
Systolic pressure
Diastolic pressure
Mean arterial pressure

A

= the hydrostatic pressure exerted by the blood against the walls of the blood vessels

Systolic pressure = higher pressure reached during systole

Diastolic pressure = lowest pressure reached during diastole

Mean arterial pressure
Not all the blood can escape to the venous system before the next beat occurs so pressure is created
= (2xdiastolic) + systolic /3
60mmHg minimum to perfuse brain
70-110mmHg normal range

41
Q

Measuring arterial pressure

A

Sphygmomanometer/pressure cuff

Fluid filled catheter

42
Q

Receptors that regulate BP

A

Baro and chemo receptors
In carotid sinus and aortic arch

43
Q

Factors affecting BP

A

CO:
Increased CO -> increased BP
Sympathetic stimulation = increases HR and force of contraction
Para = decreased HR and force of contraction

Total peripheral resistance:
Sympathetic stimulation increased BP

Blood volume viscocity:
Loss of blood leads to decreased BP
Increased viscocity leads to increased BP

44
Q

Response to haemorrhage

A

Autonomic effect on heart:
Increased HR and force of contraction
Sympathetic nervous tone increased – noradrenaline acts on B1 adrenoreceptors
Parasympathetic vagal tone decreased
Increased SV -> increased CO -> increased MAP

Neural effect on adrenal:
Sympathetic stimulation of adrenal glands
Releases adrenaline in blood
Acts on B1 adrenoreceptors

Neural effect on vasculature:
Increased sympathetic tone -> vasoconstriction
Increased systemic vascular resistance -> MAP returns to normal

45
Q

Hypovolaemia vs dehydration

A

Hypovolemia = fluid loss from vasculature
Hypovolemic shock = inadequate O2 delivery to tissues due to loss of vascular fluid

Dehydration = loss of extracellular and intracellular fluid

46
Q

Effect of hypovolaemia on cardiac function

A

Preload decreased
SV decreased
MAP decreased
Tissue oxygen delivery decreased

47
Q

How foetal ciculation differs from adult

A

Foetus breathes amniotic fluid – pulmonary artery doesn’t carry oxygen
Fetal blood is oxygen poor
Fetus swims in amniotic fluid – stable temp
Fetus is fed parentally – hepatic portal vein not needed

48
Q

Changes at parturition

A

Respiration starts
Kidneys need to rid waste
Thermoregulation begins
Digestion begins
Fetal circulation becomes closed
Ductus venosus closed – blood diverted through hepatic portal vein - due to reduction in PGE2
Foramen ovale – closes and fuses as blood is diverted to lungs rather than RV = fossa ovalis
Ductus arteriosus closes - due to reduction in PGE2

Jorge's CAR (15 decks)

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