DKHI Flashcards
Explain the following signs found when assessing patient with GI bacterial infection: Tachycardia Slow capillary refill Decreased JVP Peripheral Cyanosis
Tachycardia: inflammatory response leads to vasodilation which along with the diarrhoea leads to hypovalemia contributes to hypotension detected at baroreceptors and reflex SNS response which includes Tachycardia
Slow capillary refill: SNS mediated upstream vasoconstriction plus possible hypotension leads to decreased hydrostatic pressure in capillaries; when capillaries are emptied of blood they’ll take longer to refill
Decreased JVP: volume depletion from diarrhoea and tachycardia decreases blood volume on venous side of circulation
Peripheral cyanosis: SNS response to hypotension includes peripheral vasoconstriction; less blood flow to limbs leading to cold skin and bluish blood in capillaries; slower blood flow gives a greater time for oxygen to be extracted
Explain how improper functioning of CV centre of the brain can lead to dizziness
Less sympathetic output plus parasympathetic withdrawal in response to decreased signalling from baroreceptors leads to less blood to the head
Explain how severe stenosis of the aorta can lead to dizziness
Compromises increased cardiac output in response to sympathetic stimulation of the heart leading to less blood to the heard
Explain how anaemia can lead to dizziness
Anaemia leads to vasodilation which decreases arterial resistance making it harder to maintain arterial pressure leading to less blood to the head. Additionally less oxygen carried per unit of blood which contributes to decreased oxygen delivery to the brain.
Explain how calcium channel blockers can lead to dizziness
Causes vasodilation and can decrease conduction of electrical signals in the heart.
Describe the characteristics of a cancer cell that would enhance ability to metastasise
Capable of epithelial to mesenchymal transition
Ability to evade immune system
Change in cell surface molecules (alter cell adhesion)
Ability to increase proteinase activity (degrade proteins in basement membrane and extracellular matrix)
Ability to trigger or increase angiogenesis
Describe the mechanisms by which these signs are produced at site of a DVT:
Elevated surface temperature
Swelling
Visible venous collaterals
Surface Temperature: impaired venous drainage leads to more blood in capillaries including cutaneous ones, raising temperature.
Swelling: impaire venous drainage increases hydrostatic pressure upstream, including capillaries, imbalance in Starling forces means more fluid leaves capillaries for extravascular space leading to oedema.
Visible venous collaterals: increases hydrostatic pressure upstream, increased proportion of cardiac output flows through vessels not affected by blockage, so newly recruited veins drain more of the circulation, dilating and becoming visible
List functions of Neutrophils
Phagocytosis of pathogens, trap to impede pathogens, secretion of IL-12, secretion of B-lymphocyte stimulator, secretion of chemokine, secretion of other pro inflammatory cytokines, secretion of chimeric, activation of dendritic cells
Explain cherry red colour seen in peripheries of someone with carbon monoxide poisoning
Cherry red - reflects the content of blood flowing through cutaneous capillaries. Average affinity for oxygen is increased in Hb that has carbon monoxide bound to Hb. Less oxygen will be lost as blood flows through capillaries os the colour is unnaturally red for capillaries
Give examples of mechanisms for bacterial pathogenicity (including mechanism + bacteria that use it)
Capsule: Strep pneumonia, Neisseria meningiditis, Pseudomonas aeruginosa
Toxins: Listeriolysin O from Listeria monocytogenes; Elastase from P aeruginosa
Adherence: via fimrbiae by E coli in GIT; teichoic acids by Staphylococcus spp
Exoenzymes: Hyaluronidase from Staphylococcus aureus, or Streptococcus pyogenes
Why does Carbon Monoxide poisoning lead to acidic blood?
CO inhibits cytochrome oxidase in the ETC. Because ATP is not produced by mitochondria anymore (lack of O2 and the inhibition), the body switches to anaerobic glycolysis for ATP production. This leads to lactic acidosis - pyruvate converted to lactate which increases in blood causing acidic blood.
Why does dehydration lead to a confused state?
Change in plasma osmolality would have an adverse effect on cerebral function. As water and electrolytes can pass freely through capillary membrane, the interstitial fluid would equilibrate with the plasma and have a higher osmolality than the intracellular fluid in neutrons. Water would be drawn from the neuronal cells, causing them to shrink and interfere with cerebral function.
Why is skin turgor decreased in dehydration?
Normal skin elasticity or turgor is dependent on collagen, elastin, and fluid content. In dehydrated patients, available fluid and water in the body is reabsorbed and used to supplement circulating volume. So, fluid is drained from these layers during dehydration and results in the decreased skin turgor.
What is isosmotic dehydration?
Occurs when water loss is directly related to salt loss, so there is a loss of isosmotic fluid. The loss is limited to the extracellular space. There is no major change in osmolality of the ECF, therefore any shifts in fluid are into or out of the ICF.
Cardiac output is decreased and as a result some changes in blood distribution in particular organs appear.
Causes include: GIT disease, assimilation of fluid in abdominal cavity or intestine fistulae
What is hypo-osmotic dehydration?
When electrolyte loss exceeds water loss.
Because the ECF osmolality drops compared to that of the ICF, water moves from the ECF into the ICF and thus concentrates the ECF. Cells become swollen.
Symptoms: (as a result from decrease ECF and loss of Na+) weakness, sunken eyes, low skin turgor, low blood pressure, thready pulse
Causes: chronic pyelonephritis, polyuria, chronic adrenal insufficiency, encephalitis
What is hyper osmotic dehydration?
When water loss exceeds electrolyte loss.
ECF osmolality rises compared to ICF, so fluid transfers from cells to ECF. Results in a decrease of both ICF and ECF compartments with high osmolality.
Causes: low water intake (unconsciousness, absence of thirst, swallowing disorders), high water loss (sweating, polyuria, diabetes)
Outline how the following conditions lead to secondary hypertension and tests to diagnose: Hyperaldosteronism Pheochromocytoma Cushing Syndrome Amphetamine drug use
Hyperaldosteronsim:
excess aldosterone stimulates sodium potassium pump which reabsorbs sodium and thus water to increase plasma volume. Also leads to metabolic alkalosis (loss H+ when low potassium for the Na+/K+ pump as well as bicarbonate reabsorption); and hypokalaemia as potassium is excreted in exchange for sodium
Test via serum potassium levels and renin/aldosterone ratios
Pheochromocytoma:
Tumour leading to high levels of catecholamines (adrenaline and noradrenaline). Leads to increase heart rate via beta-1 receptors and vasoconstriction via alpha receptors which increase blood pressure.
Test via catecholamine levels in urine.
Cushing’s syndrome:
Excess cortisol production which leads to hypertension in 2 ways. Cortisol increases sensitivity of blood vessels to catecholamines leading to vasoconstriction. Cortisol mimics mineralocorticoids like aldosterone which can then lead to hypertension even though aldosterone levels are actually low.
Test via cortisol excretion in urine
Amphetamine in urine:
Amphetamine blocks the reuptake of catecholamines by neutrons so accumulation of these at the synaptic cleft leading to excess SNS activation (vasoconstriction and increased CO).
Explain in terms of blood flow and oxygen delivery why a patient with a left to right cardiac shunt develops SOB on exertion.
With a left to right shunt, some of the blood that would orginarily go into the left ventricle goes into the right atrium during atrial contraction.
Consequently, although there is plenty of oxygen carried per unit of blood, the delivery of blood to the tissues is attenuated which limits oxygen delivery.
Explain in terms of blood flow and oxygen delivery why a patient develops SOB on exertion with a right to left cardiac shunt.
There is plenty of blood coming out of left ventricle but it is mixed with deoxygenated blood from the right side of the heart. Consequently, the mixed arterial blood has less oxygen to deliver and shortness of breath accompanies the extra oxygen demand with exertion.
