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