PME2 Pathophysiology

Question 1

Acute Thoracic aortic Dissection Pathophysiology

Answer 1

Constant high pulsatile pressure weakens tunica intima

blood flows into the intima-media space

false lumen created

can move distally or proximally

can be partial or complete

complete creates true lumen collapse

most common in ascending aorta

will affect left or right coronary artery

Question 2

Addison Disease Pathophysiology

Answer 2

adrenal glands don’t release aldosterone cortisol and adrenal androgens to meet physiologic needs, despite release of ACTH from the pituitary

Question 3

Adrenal Gland Physiology

Answer 3

hypothalamus wakes up the pituitary gland

pituitary gland releases hormones telling adrenal glands to release cortisol and aldosterone

cortisol and aldosterone travel through blood and tell kidneys to react to stress

Question 4

Aortic Aneurysm Pathophysiology

Answer 4

degeneration, of the aortic wall caused by:

smooth muscle cell depletion and disorganisation

elastic fiber fragmentation

excessive deposits of collagen and proteoglycans

allowing the aorta to increase in size and possibly rupture

Question 5

Allergy Pathophysiology

Answer 5

Antigen exposure

TH2 cells produce antibodies

Hypersensitivity reaction produces IgE antibodies

IgE antibodies attach to FCεRI receptors
(on Eosinophils, Mast cells and Basophils)

IgE coated cells now sensitised to antigen

No allergic response occurs

(Molecule capable of inducing allergic response)

Question 6

Anaphylaxis Pathophysiology

Answer 6

Histamine causes Nitric Oxide synthesis leading to systemic vasodilatation

Increased vascular permeability

Bronchial smooth muscle contraction

Increased mucus secretion

Leukotrienes contribute to bronchial smooth muscle contraction

Platelet Activating Factor & CysLTs cause urticaria & erythema

Prostaglandins regulate smooth muscle contraction

Histamine causes GIT symptoms of abdo pain/cramping and nausea and vomiting

Question 7

asthma pathophysiology

Answer 7

immune system activated inflammatory mediators released inflammation of lower airway causing irritation and mucosal oedema causing turbulent air flow bronchoconstriction increases residual volume, PCO2, air trapping and alveolar pressure and reduces oxygen rich air to alveoli causing decreased blood oxygenation

Question 8

Body’s Response to Profound Dehydration

Answer 8

cerebral perfusion pressure decreases

Blood volume decreases

Preload decreases

BP falls

Heart rate increases

Question 9

Cardiovascular Pathophysiologic Response to Acute Pulmonary Embolism

Answer 9

Increased pulmonary vascular resistance and pushing back into RV

Increased right ventricular dilation

Decreased right ventricular contractility and output
(RV not as strong as LV)

Decreased left ventricular preload, therefore low cardiac output

Decreased Systemic BP

Decreased RV coronary perfusion
(as less blood available)

Decreased O2 delivery to right ventricle

Obstructive shock
(secondary to PE)

Death

Question 10

Function of adrenal androgens

Answer 10

no known physiologic role

mediate some secondary sexual characteristics in women (e.g, pubic and axillary hair)

overproduction may result in virilism

Question 11

Function of Glucocorticoids

Answer 11

primarily cortisol

carbohydratemobilizing activity

ubiquitous physiologic regulators influencing a wide variety of bodily functions

Question 12

Function of Mineralocorticoids

Answer 12

principally aldosterone

regulate renal sodium retention influencing electrolyte balance, intravascular volume, and blood pressure

Question 13

How do pH changes affect potassium?

Answer 13

Hydrogen ions accumulate in the intracellular fluid (ICF) during states of acidosis

K+ shifts out to maintain a balance of cations across the membrane

Question 14

How does the hepatic portal system work?

Answer 14

blood flows through spleen, pancreas, gut, intestines

goes through portal vein into liver

sinusoids filter and remove toxins and bacterias

store up to 75% of proteins and carbs

1L blood per minute through liver, inferior vena cava and then through arterial system

3mmHG of pressure in portal system - easy to be damaged

Question 15

Hyperkalaemia Pathophysiology

Answer 15

Membrane hypopolarisation causes an increase in neuromuscular excitability

Question 16

Hypokalaemia Pathophysiology

Answer 16

membrane hyperpolarisation causes a decrease in neuromuscular excitability (resting membrane potential is lower)

Question 17

Nephrolithiasis (kidney and ureteral stones) Pathophysiology

Answer 17

calcium oxalate or calcium phosphate erodes through and creates a plate which gets bigger and stays in kidney or moves

Question 18

Pathophysiology of Autonomic Dysreflexia

Answer 18

• nociceptors stimulated below T6
• lateral spinothalamic tract carries message to T6 where cord severed
• creates overexaggerated reflex stimulus by simpathetic nervous response
• leads to massive arterial resistance (constriction) due to splantnic circulation (abdomen supply)
• 1/4 blood volume sent to below T6
• arterial constriction causes massive significant rise to system BP resulting in vasalspasm hypotension and pallor of skin
• BP stimulates baroreceptors in carotids
• message sent to CNIX and CNX to try to reduce BP, leading to vasodilation above T6 and reflex bradycardia and flushed skin, headaches
• uncontrolled hypertension as splantnic circulation not controlled

Question 19

Pathophysiology of Bowel Obstruction

Answer 19

Obstruction

Dilation due to air and gas

wall swells

Bowel absorption function reduced

Fluid sequestered into the lumen

Ischemia

Necrosis

Perforation

Question 20

Pathophysiology of DKA

Answer 20

glucose not converted to energy as not enough insulin or insulin resistance which increases BGL (glucose can’t get into cell)

fat breakdown for energy produces ketone acids

metabolic acidosis develops when BGL extremely high

kidney produces excess urine causing polyruia and thirst

person can’t drink enough to maintain fluid levels causing dehydration and hypovolaemia

respiratory rate increases to blow off excess CO2 caused by ketones

Question 21

Pathophysiology of Gall Stones

Answer 21

too much cholesterol or not enough bile salts that allow cholesterol to crystalise and form gall stones (biliary calculi)

Question 22

Pathophysiology of Central Vertigo

Answer 22

Issue with vestibular Occular Reflex:

Vestibular nuclei in brainstem

Cerebellum (voluntary movement,coordination, balance, speech)

Parietal lobes (proprioception and visualinfo)

Question 23

Pathophysiology of meningococcal septicaemia

Answer 23

bacteria changes permeability structure and degrades endothelial cells leading to fluid and electrolyte loss into interstitial space causing severe
hypotension and decreased cardiac output

Question 24

Pathophysiology of migraine headache

Answer 24

neurons in trigeminovascular system triggered
neuropeptides increase and act on mast cells
peripheral and central sensitization
migraine

Question 25

Pathophysiology of MODS

Answer 25

infection penetrates the blood systemic inflammation response vasodilation and capillary permeability causing relative hypovolemia whilst vascular damage causes DIC and rash MODS acidosis death

Question 26

Pathophysiology of normal response to a stimulus

Answer 26

stimulus nociceptor - pain receptor peripheral nerve - afferent pain fibre (dorsal ganglion and dorsal root) synapse spinal decussation lateral spinothalamic tract (pain) reticular formation (in pons and medulla - awareness, alert) thalamus (sensory relay centre) somatosensory cortex - parietal lobe - locate pain hypothalamus - stress response (sympathetic) limbic system - emotional response

Question 27

Pathophysiology of Pancreatitis

Answer 27

large pooling of pancratic juices in the pancreas which overwhelms trypsin inhibitor too much trypsin in pancreas will start eating pancreas can cause multi organ dysfunction secondary to cytokine cascade death occurs rarely

Question 28

Pathophysiology of perciardial effusion and cardiac tamponade

Answer 28

stretch is speed dependent, eg: slow effusion = > ability to stretch effusion results in too much fluid in pericardial cavity increases pericardial pressure cardiac tamponade results when increased pericardial pressure creates cardiac dysfunction

Question 29

Pathophysiology of Peripheral Vertigo

Answer 29

Vestibular system Cranial nerve VIII

Question 30

Pathophysiology of portal hypertension

Answer 30

restricted blood flow, leading to increase in pressure leading to oesophageal varices and varices ascites

Question 31

Pathophysiology of protein breakdown

Answer 31

acinar cells release trypsinogen and trypsin inhibitors in pancreas go through pancreatic duct into duodenem then transformed into tryptin by enteropeptidase which removes amino acids and creates trypsin to break down proteins trypsin activated peptide can then be used as a tool to screen for pancreatitis

Question 32

Pathophysiology of Rabdomyolysis

Answer 32

bilipid layer of cell impermable to K and NA Sodium K pump keeps concentration gradient in homeostasis pump fails and lets K leak out of the cell causing hyperkalaemia sodium enters cell taking a lot of water with it and cell ruptures

Question 33

Pathophysiology of renin angiotensin system shock compensation

Answer 33

kidneys pick up drop in BP Renin release converts angiotensin 1 to angiotensin II in lungs II is potent vasoconstrictor, increases antidiuretic hormones and aldosterone (to increase water uptake)

Question 34

Pathophysiology of Second Contact with Antigen

Answer 34

Antigen binds to sensitised IgE Activates signalling cascade Eosinophils, Mast cells & Basophils degranulate ``` Release cellular inflammatory mediators Histamine Platelet Activating Factor CysLT Tryptase Prostoglandins Cytokine/Chemokine ``` Allergic response occurs

Question 35

Pathophysiology of Sepsis

Answer 35

Infection penetrates the blood causing dysregulated inflammation response and body is overwhelmed by release of anti-inflammatory mediators increasing vascular permeability causing fluid shifts and cellular hypoxia. Fluid loss into interstitium causes increase in peripheral vascular resistance worsening tissue ischemia and increasing lactate. Within sepsis response microcirculatory dysfunction resulting in circulatory dysfunction and DIC)

Question 36

Pathophysiology of Septic Shock

Answer 36

sepsis not treated cardiac output decreases, BP falls (with or without an increase in peripheral resistance) causing typical features of shock Vasoactive mediators cause blood flow to bypass capillary exchange vessels (a distributive defect) Poor capillary flow from this shunting and capillary obstruction by microthrombi decreases oxygen delivery, impairing removal of carbon dioxide and waste products Decreased perfusion causes dysfunction and sometimes failure of one or more organs, including the kidneys, lungs, liver, brain, and heart

Question 37

Pathophysiology of shock

Answer 37

after initial injury HR increases to maintain volume circulating As HR gets faster (\>150/180), myocardium won't stretch and preload not there BP declines as HR can only do so much refractory shock death

Question 38

Pathophysiology of Nonperforated and Perforated Appendicitis

Answer 38

lumen obstructed by faeces, tumour, foreign body E. coli and bacteroids fragilis overgrowth causing secretions secretions don't drain, intraluminal pressure increases venous and arterial blood flow restricted, mucosa ulcerates, bacteria causes inflammation and oedema, restricted blood flow causes tissue death and gangrene appendix splits open and faecal matter leaks into perineum

Question 39

Pathophysiology of Hyperosmolar hyperglycaemic syndrome (HHS)

Answer 39

insulin can't get into cell due to insulin resistance BGL increases enough sugar getting into cell to provide energy, therefore no fat breakdown (keto acidosis) big cells draw fluid into circulation to help dilute glucose levels diuresis occurs

Question 40

Pneumonia Pathophysiology

Answer 40

pathogen multiplication - invade from naso or oropharyngeal pathway and aspirate into lungs local inflammation - macrophages overwhelmed, cytokines create inflammation and increase microvascular permeability and flooding of WBC into alveolar space causing diffusion issue systemic inflammation - cytokines in alveolar space spread into systemic system creating systemic response of increased WBC, temp, cardiac output dysregulation

Question 41

Potassium Notes

Answer 41

Major intracellular cation 90% Concentration maintained by Na+/ K+ pump Regulates intracellular Na+ and H+ electrical neutrality Transmits and conducts nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction

Question 42

Respiratory Pathophysiologic Response to Acute Pulmonary Embolism

Answer 42

V/Q mismatch dead space

Question 43

Splantnic Circulation Pathophysiology

Answer 43

blood flows through spleen, pancreas, gut, intestines then goes through portal vein into liver sinusoids filter and remove toxins and bacterias, store up to 75% of proteins and carbs Liver has 1L blood flow every minute then through inferior vena cava and then through arterial system

Question 44

Vertigo Pathophysiology

Answer 44

mismatch between visual, proprioceptive and vestibular inputs

Question 45

What causes lysis?

Answer 45

Anaerobic metabolism ATP Chemotherapy Major Burns Rabdomyolysis Sodium potassium pump

Question 46

What do prostaglandins do?

Answer 46

inhibit acid secretions and stimulate mucous production and bicarbonate and protect against damaging compounds

Question 47

What happens to potassium in cell lysis?

Answer 47

potassium leaks out of the cell

Question 48

What happens when the portal system gets to 10 mmHG or more?

Answer 48

oesophageal varices and varices ascites develops

Question 49

What influences serum potassium levels?

Answer 49

Aldosterone Catecholamines Insulin renal regulation of potassium secretion

Question 50

What is the digestive process?

Answer 50

mouth - mechanical breakdown propulsion due to peristalsis in oesophagus and bowel digestion within small bowel (pancreas helps) defecation

Question 51

What is the hormonal control of extrinsic control in renal filtration?

Answer 51

renin angiotensin system: renin (enzyme) secreted by juxtoglomerular cells converts angiotensinogen to angiotensin I angiotensin converting enzyme transforms angiotensin I into angiotensin II, stimulating aldosterone in adrenal glands causing sodium reabsorption, which draws in water to increase blood volume and increases systemic blood pressure

Question 52

What is the pressure of the portal system?

Answer 52

3 mmHG

Question 53

What is the role of potassium K⁺?

Answer 53

major intracellular cation Concentration maintained by sodium/Potassium pump Regulates intracellular electrical neutrality in relation to Na+ and H+ Essential for transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction | (90-98% inside cell)

Question 54

Cardiogenic APO Pathophysiology

Answer 54

1. The left ventricular fails 2. Congestion of the pulmonary vasculature=increased hydrostatic pressure 3. Overwhelmed osmotic/oncotic pressure (homeostatic forces are no longer equal) 4. Plasma is fored through the vessel wall into the interstitial space then to the alveoli 5. The surfactant that holds the alveoli open is diluted and the alveoli collapse 6. Gaseous echange is severly limited then hypoxia rapidly ensues