Basic Science MRCS Physiology Flashcards
Which body parts have higher temperatures on measurements
Rectal 0.5 higher than Mouth and axilla
When is temperature highest in menstrual cycle
0.5 higher in latter half
Sx of hypothermia
Bradycardia
Hypotension
Resp depression
Muscle stiffness
VF
Vessel Reflex to hot/cold stimulus
Cold- vasoconstriction on ispilateral and contralateral side
Afferent- cutaneous nerve
Centre- hypothalamus and spinal
Eff- symp
Hot- vasodilation
Centre- above c5
Reduced symp activity
Water composition of human
Of 70kg man -2/3 is water - 44kg
2/3 intracellular- 25kg
1/3 extracellular- 19kg
Of that 2/3 interstitial - 15L
intravascular 3L
Transcellular 1L
Water loss compostion
Resp 500
Urine -500
Skin- 400
Faeces-100
Which is triggered first ADH or thirst
ADH- low osmolality threshold of around 10
So triggered before getting thirsty
Triggers for thirst and ADH
Osmolality receptors
Baroreceptors- carotid and aortic
Reduced CVP- atrial
Angiotensin 2 in brain
ANP action
Increasing GFR
Inhibiting Na reabsorption in CD
Reducing secretion of renin and aldosterone
Water excess clinical manifestation
Primary- low osmolality- water intoxication
Secondary due to high sodium- oedema
Water depletion clinical manifestation
Primary- loss of water- high osmo- thirst
Secondary- loss of Na- circulatory collapse
ECG of hyperkalaemia and hypo
Hyper- broad QRS, flat p, tinted T
Hypo- Peaked P, flat/inverted T
Important buffer systems in body
Proteins- helps with pH ICF and ECF
Hb
Phopshate- of ICF and urine
Bicarbonate- most important in ECF
Cause of resp acidosis
CNS depression
Neuromuscular dise3ase
Skeletal disease
Impaired gas exchange- obstructive airway, alveolar disease- pneumonia, ARDS
Cause of resp alkalosis
High altitude
Pneumonia
Pul Oedema
PE
When is BE -/+
BE + in metabolic alkalosis
-in metabolic acidosis
24 hours maintainence fluids for uncomplicated patient
2L dextrose
1L NaCl
60mmol of KCL
Physiological response to surgery
Released catecholamines
Increased cortisol and aldosterone
Retention of Na- reduced urine
RAS activated
ADH released
K usually doesnt fall but might rise do to tissue damage
When is HAS used
Severe hypoproteinaemia in renal or liver disease
Large volume paracentesis
Massive liver resection
Problems with plasma expanders
Dilution coagulopathy
Allergic
Dextran intereferes with cross matching
Where does IV fluids go after administration
2/3- ECF
1/3- ICF
Tidal volume amount and changes in exercise
500ml
Goes up to 2-3L in exercise
Normal intrapleural pressure and during exercise
Beginning of inspiration-4
End -9
Exercise -30 in inspiration
+20 on expiration
Expanding lungs with air vs saline
Lack of surface tension with saline- greater compliance
Only opposing force is elastic tension
Surfactant functions
Lower surface tension- increase compliance- reduce work of breathing
Prevent fluid accumulation
Reduce tendency to collapse
Law of laplace in alveoli
Laplace
Alveolar pressure= 2 Tension/R
So smaller alveoli more prone to collapse - since generate larger pressure causing air to travel to larger alveoli
Therefore smaller alveoli have more surfactant to lower their Tension more
Compliance calculation
change in volume/change in pressure
Cause of increase/decrease in compliance
Increase- emphysema due to destruction of elastic tissue
Decrease- fibrosis, oedema, reduced surfactant, supine, mechanical ventilation due to reduced blood flow
Main resistance of air flow
1/3 nose, pharynx, larynx
2/3-tracheobronchial tree
little distally
Elastance equation
Change in pressure/change in volume
How to calculate FRV/RV
Helium dilution method
How to calculate anatomical dead space
Fowler method- breath of pure O2
nitrogen components measured - as alveolar has nitrogen from old breathing
Calculated from Bohr equation
Factors increasing anatomical vs physiological dead space
Anatomical- increase size of patient
Standing
Bronchodilation
Physiological
Hypotension
Hypoventilation
Emphysema and PE
PPV
Measuring closing capacity
Volume at which small airways at base start to close
Usually 10% of VC
Breathes out to FRC- takes 100% O2
Point between phase 3+4 on curve- there is an increase in 4 as only the poorly ventilated upper lobes are open
Flow volume curve characteristics with diseases
Obstructive- concave expiration phase
Restrictive- normal shape, volume lower
Which part of the lung has the lowest ventilation
Apex
Due to weight- causing pleural fluid - more negative intrapleural pressure and compliance differences
Determinates of pulmonary blood flow
Hydrostatic pressure in PA
Pressure in PV
Pressure of air in alveoli
Blood flow in zones of lungs
1- apex- alveolar pressure similar to PA- smaller vessels compressed- low flow
2-PA is higher- increased flow
3- PA greatly exceeds
These are only true with standing up
Change in pressure in Pul arterioles in excerise
Changes very little
Due to increase in CO
Causes Recruitment of additional vessels- many caps at rest closed
Vessels getting distended
V/Q ratio throughout lung
3 at apex- ventilated more than perfused
2/3 up chest-1
Base- 0.6- better perfused than ventilated
Stages of pulmonary oedema development
Interstitial oedema- doesnt affect ventilation at first- but once large enough to affect lymph to cause alveolar oedema
Alveolar oedema- fill with fluid- increasing surface tension and shrinking alveoli
leading to vasoconstiction due to hypoxia
Airway oedema- causing blood tinged frothy sputum
Diagnosis of ARDS
Known cause
Acute
Fluffy infiltrates
PWP- <18
Stages of ARDS
1- Intially active exudate- inflammtory mediators, proteases
Damage lung and Increase cap perm
Thrombosis and haemorrhage in alveolar capillaries- alveolar collapse - decreased lung compliance
2-Regeneration of type 2 pneumocytes- organisation with fibrosis, and obliteration of alveolar space
Factors affecting gas diffusion
Pressure gradient - partial pressure
Diffusion coefficient- how well it can diffuse- determined by solubility and molecular weight
Tissue factors- large SA, short diffusion distance -
Diffusion distance constituents
Pulmonary surfactant
Alveolar epithelium
BM
Pulmonary endothelium
Examples of pulmonary shunting
Travel through lungs without contact with ventilated alveoli
Bronchial veins
Pneumonia
Fetal and myoglobin oxygenation curve
Fetal comprimised of 2a 2y- shift to left
Myoglobin- even further left to provide additional O2 in anaerobic
Transportation methods of CO2
HCO3- 60-70% formed in red cell and diffuses out- Cl- replaces it in red cell- reversed in alveoli
Carbamino- between proteins mostly globin- 20-30%
Dissolved 10%
Difference between O2 and CO2 dissociation curve
Co2 solubility greater
Normal range of PaCo2 smaller
Blood cannot be saturated with CO2- so no plateau
Haldane effect
CO2 carried increases as O2 levels fall
At given partial pressure Co2 carried increases
Chemoreceptors of respiratory regulation
Central- close to medulla
Change relative to pH
Increase resp rate if CO2 increases
Peripheral
Carotid bifurcation and aortic arch
pH and PO2
Only PO2 when abnormally low- <8
Hering Bruer reflex
Strech receptors in lung - prevent over inflation via vagus
Carotid bodies CV response to hypoxia
Increased HR
Increased CO
Vasoconstriction in skin and splanchnic
Physiological alterations with chronic hypoxia
Increased minute volume
RBC
CO
Vascularity of organs
Complications of mechanical ventilation
*ventilator-induced injury
*volutrauma
*barotrauma
*hypotension and decreased cardiac output: decreased venous return due to positive intrathoracic pressure
*respiratory muscle atrophy
*nosocomial infections
*technical complications, e.g. disconnection
*increase in intracranial pressure (ICP) due to the increase in intrathoracic pressure.
Modes of ventilation
Controlled mandatory ventilation- no resp effort- set volume
Synchronised intermittent MV- less sedation- some breath initiated by patient
Pressure controlled ventilation- reduces risk of barotrauma
Pressure support ventilation- used in combo- allows weaning by triggering breath
Calcium in cardiac contraction
In the absence of calcium the troponin/tropomysin complex inhibits cross-bridging between actin and myosin filaments.
*When calcium binds to troponin, formation of cross-bridging occurs between the filaments. The filaments then slide over one another to cause contraction
Mechanism of contraction in cardiac cells
Arrival of the action potential allows Ca2+ to move from the sarcoplasmic reticulum into the cytoplasm.
*Ca2+ binds to troponin C, eventually activating the actin–myosin complex, resulting in contraction.
*The plateau phase, the result of further calcium influx, prolongs and enhances contraction.
*The cardiac action potential is very long (200–300 ms). After the contraction there is a refractory period when no further action potentials can be initiated and therefore no contraction occurs. The long action potential and refractory periods ensure contraction and relaxation of the heart, allowing the chambers to fill during relaxation and empty during contraction.
*Intracellular Ca2+ is the most important factor controlling myocardial contractility:
*increased intracellular Ca2+ increases force of myocardial contraction
*decreased intracellular Ca2+ decreases the force of myocardial contraction
Location of SA and AV node
SA- right atrium near SVC entrance
AV_ fibrous ring on right side of atrial septum
Properties of SA, AV node and purkinje
Ability to depolarise at regular intervals- self excitation
Long refractory period- so cells with highest frequency (SA node) control HR
Normal pressure in heart
RA- 0-4
RV- 25/0-4
PA- 25/15
LA-5-10
LV- 120/0-10
EF calculation
EF= SV/LVEDV
Which JVP wave is synchronous with carotid pulse
C wave
Factors affecting coronary blood flow
Coronary flow occurs mainly during diastole.
*Conditions resulting in low diastolic BP or increased intramyocardial tension during diastole (e.g. an increased end diastolic pressure) may compromise coronary blood flow.
*Subendocardial muscle, where the tension is highest, is particularly vulnerable.
*Diastolic time is important. At fast rates, inadequate myocardial perfusion occurs.
Factors affecting pre load
*venous return
*atrial systole (fibrillation)
*myocardial distensibility
How to measure pre load
central venous pressure (CVP)
*pulmonary artery occlusion pressure (PAOP).
What increases after load
*raised aortic pressure
*aortic valve resistance (aortic stenosis)
*ventricular cavity size; increased ventricular volume; requires greater tension to contract (Laplace’s law)
*raised systemic vascular resistance (SVR), e.g. shock
Ficks law
Amount of substance taken up by an organ per unit time is equal to the blood flow multiplied by the difference in concentration of that substance between arterial and mixed venous blood.
Factors affecting systolic and diastolic
Systolic pressure increases when there is an increase in:
*stroke volume
*ejection velocity (without an increase in stroke volume)
*diastolic pressure of the preceding pulse
*arterial rigidity (arteriosclerosis).
Diastolic pressure increases when there is an increase in:
*total peripheral resistance
*arterial compliance (distensibility)
*heart rate.
When would CVP not reflect filling pressure of left heart
If disparity between right and left ventricles
Right infarction
PE
LV disease
PAOP
Estimates LA pressure
Can estimate CO from catheter
Problems with pulse oximetry
*irregular pulse: atrial fibrillation
*venous pulsation (tricuspid incompetence)
*hypotension
*vasoconstriction
*abnormal Hb (carboxy-), and methaemoglobin
*bilirubin
*methylene blue dye
Isoprenaline effects
B effects only
Vasodilation in skeletal muscle- reduce SVR
Tachycardia
Use in HB while awaiting pacemaker
Dobutamine effects
B1 and 2
Increased HR and contraction
Mild vasodilation
Cariogenic shock- with low dose dopamine
Dopamine effects
Low dose- dilates renal, cerebral, coronary, splanchnic - via D1+2
and B1 increases contractility and HR
High dose- a-vasoconstriciton
Dopexamine effects
B2 and D
mild-Inotrope, chronotrope
Peripheral vasodilator
Phosphodiesterase inhibitor
Decrease the rate of breakdown of cAMP by phosphodiesterase III.
Increased contractility with reduced PAOP and SVR
Auerbach and Meissners plexus location and function
Myenteric (auer) lies between circular and longitudinal - motor
Meissner- submucosa- sensory
Para vs symp effect on enteric system
Symp- vasoconstriction
Inhibit glandular secretion
Contract sphincters
Inhibits muscle- motility
What types of saliva is excreted from each gland
Parotid- watery- amylase and IgA
Submandibular- 70%, mucous
Sublingual- mucoproteins 5%
Formation of saliva
Isotonic fluid secreted by acinar component
As moves along duct- NaCl removed
K HCO3 added
During high rates of secretion- Na Cl HCO3 more concentrated
Factors preventing reflux
the right crus of the diaphragm compresses the oesophagus as it passes through the oesophageal hiatus
*the acute angle at which the oesophagus enters the stomach acts as a valve
*mucosal folds in the lower oesophagus act as a valve
*closure of the sphincter is under vagal control- physiological sphincter
Where cells are located in stomach
fundus and body: peptic and parietal cells predominate
*antrum and pylorus: parietal cells are less common; mucus and neuroendocrine (secreting gastrin) cells predominate
*cardia: gastric glands are composed almost completely of mucus cell
How HCl is pumped in/out of parietal cells
H+ ions are pumped from the cell by the H+/K+ ATPase system.
*Cl− ions are pumped from the cell by two routes: one is a chloride channel, the other is a Cl−/K+ co-transport system (K+ is thus cycled into the cell via the H+/K+ ATPase system and out via the Cl−/K+ system).
What protects gastric cells from digestion
Mucus secretion barrier over gastric epithelium
Alkaline
Tight epithelial junctions
prostaglandin E secretion has a protective role by increasing the thickness of the mucus layer, stimulating HCO3− production and increasing blood flow in the mucosa (bringing nutrients to any damaged areas).
Phases of gastric secretion
Cepahlic- 30%- sight and smell
VIa- Ach from Vagus
Gastrin from G cells
Histamine from mast cells- stimulate H2
Gastric- 60%- food entering
Ach
Intestinal- presence in duodenum-5%
Releases Gastrin
Other factors influencing gastric sectretion
*the secretion of gastrin is inhibited when the pH falls to around 2–3
*somatostatin secreted from neuroendocrine cells (D-cells) inhibits gastrin secretion
*secretin from the duodenal mucosa is released in response to acid in the duodenum; it inhibits gastrin release
*fatty food in the duodenum leads to the release of CCK and GIP; both inhibit gastrin secretion.
Factors determining food allowed into duodenum
-gastric volume:↑volume then more rapid emptying
*fatty food: CCK and GIP are released by the small intestine in response to fatty foods; they increase contractility of the pyloric sphincter
*proteins: proteins and amino acids stimulate gastrin release; gastrin increases contractility of the pyloric sphincter
*acid: acid entering the duodenum results in a vagally mediated delay in gastric emptying and also leads to secretin release. Secretin inhibits antral contractions and increases contractility in the pyloric sphincter. Secretin also stimulates HCO3− release from the pancreas to neutralize the acid
*hypertonic chyme: delays gastric emptying.
Drugs that reduce acid secretion
H2 receptors- cimetidine- block H2 on parietal
PPI- block H/K
Activated in acidic pH
3 types of mucosal protectants
*sucralfate: formed from sulphated sucrose and aluminium hydroxide, it polymerizes at pH < 4 to form a sticky layer that adheres to the base of the ulcer
*bismuth chelate: acts in a similar manner to sucralfate; in addition it has been shown to eradicate Helicobacter pylori
*misoprostol: a synthetic analogue of prostaglandin E2. This prostaglandin is thought to protect gastric mucosa by stimulating the secretion of mucus and bicarbonate, and increasing the mucosal blood flow.
Examples of antacids
*sodium bicarbonate
*magnesium hydroxide and magnesium trisilicate
*aluminium hydroxide.
Post gastrectomy syndrome
Iron- wrong state for absorption
B12
Billious vomittng
Dumping
Diarrhoea
Infection- reduced ability to destroy bacteria
Carcinoma
Effects of vagotomy
*Reduced gastric acid secretion.
*Delayed gastric emptying.
*Failure of the pylorus to relax prior to gastric peristaltic wave.
*Reduced pancreatic exocrine secretions.
*Diarrhoea secondary to loss of vagal control of the small bowel.
*Increased risk of large bowel cancer due to excessive bile salts reaching the colon.
What is contained in the crypts of Lieberkuhn
*undifferentiated cells that constantly replace enterocytes
*Goblet
*Paneth
*D-cells: produce somatostatin
*S-cells: produce secretin
*N-cells: produce neurotensin
*Enterochromaffin cells: produce 5-hydroxytryptamine.- serotonin
Brunners gland
Only in duodenum
Secrete bicarbonate rich mucus
Brush borders enzymes
*disaccharidases: maltase, sucrase
*peptidases
*phosphatases
*enteropeptidase or enterokinase (activates pancreatic trypsinogen)
*lactase (under 4 years).
Absoption of monosaccharides
Glucose and galactose via Na dependent
Fructose independent
Fat absorption
Coated in bile salts in duodenum - smaller droplets
Lipases- monoglycerides and FFA
These combine with bile salts to form micelles
Diffused into enterocyte- bile salts stay in lumen
SER- reforms Triglycerides- formed into chylomicrons- diffuse into lacteals - then return to venous
How vitamins are absorbed
C- by Na dependent in jejunum
B12- IF- ileum
Remaining B diffuse freely
ADEK- micelles
How is iron absorbed
Duodenum and jejenum in Fe2+ not 3+
Gastric acid responsible for converting
Absorbed by transferrin
Into by endocytosis then to plasma
Movement in small bowel
Segmentation- circular muscle- circular movement of chyme
Peristalsis- propulsion triggered by distention- longitundinal muse
MMC- contraction across full length of small bowel, lasts several hours- move remaining food to colon
Reflexes affecting intestinal contractility
*ileogastric reflex: distension of the ileum decreases gastric motility
*gastroileal reflex: increase in gastric secretion or contractility increases ileal motility.
Effect of duodenal resection
Ulceration of small bowel- no Brunner gland
Malasorption- Fe, Ca, P
Dumping
Effects of Terminal ileal resection
Decreased Bile salt reabsorption- more gallstones
Bile salts in colon- malignancy
B12 def
reduced water reabs- diarrhoea
Fluid secretions of pancreas
Epithelial cells- HCO3 secreted in exchange for Cl
Na K exchanged for H formed by carbonic anhydrase
What activates trypinogen
Enterokinase- secreted by duodenum
What dose trypsin do
Activates other enzymes
*chymotrypsinogen: chymotrypsin (cleaves peptide bonds)
*proelastase: elastase (cleaves peptide bonds)
*trypsinogen: trypsin (cleaves peptide bonds)
*procarboxypeptidase: carboxypeptidase (cleaves peptides at the C-terminus).
Action of amylase
starch digestion; it splits α-1,4-glycosidic bond
Lipolytic enzymes examples and what activates them
Tyson actviates
Lipase- TG- to FFA and glycerol
Co lipase- binds lipase to lipids
Phospolipase- FFA from PL
Cholesterol esterase
Regulation of pancreatic secretions
Cephalic- vagal
Gastric- vagal
Intestinal- CCK and secretin
CCk- release of fluid rich in enzymes from acing cells
Secretin- bicarb rich
Lipid and peptides- increase CCK
Acid- secretin
% of bile acids reabsorbed and location
> 90% of secreted bile is absorbed in distal ileum
Livers role in protein metabolism
gluconeogenesis- produce glucose form amino acids
Synthesises albumin, clotting factors
Handles degradation products such as ammonia- converted to urea
Liver role in fat metabolism
Glucose is converted to FFAs; this is then transported to adipose tissue. It is then combined with glycerol and stored as triglycerides. During starvation these stores are released, providing fatty acids (provides energy as ATP for gluconeogenesis) and glycerol (acts as a non-carbohydrate substrate for gluconeogenesis)
*synthesizes lipoproteins and cholesterol
Which substances does liver detoxify
*peptide hormones: insulin, Anti-Diuretic Hormone (ADH), growth hormone
*steroid hormones: testosterone, oestrogen, adrenal cortex hormones
*catecholamines
*drugs
*toxins.
Via-1- increasing water solubility via p450
2- reducing biological activity
What does the liver store
Iron
Copper
Vit ADEK, B12
Glycogen
Fats
Cells in hepatic sinusoids that phagocytose
Kupffer cells
Biochem findings of prehepatic jaundice
*no bilirubin in the urine (unconjugated bilirubin is not water-soluble)
*↑urobilinogen in the urine (as a result of more bilirubin being broken down in the intestine)
*reticulocytosis: in response to the need to replace destroyed blood cells
*anaemia
*↑lactate dehydrogenase (LDH)
*↓haptoglobin: protein that binds free haemoglobin and transfers it to the liver.
Cause of congenital hyperbilirubinaemia
unconjugated hyperbilirubinaemia:
*Gilbert’s syndrome: due to an abnormality in bilirubin uptake
*Crigler–Najjar syndrome: due to the absence of glucuronyl-transferase
conjugated hyperbilirubinaemia:
*Dubin–Johnson and Rotor’s syndrome: defects in the handling of bilirubin.
Lab findings of hepatocellular jaundice
*liver enzymes, i.e. ↑ aspartate amino transferase (AST) and ↑ alanine amino transferase (ALT); this reflects liver damage and thus release of these enzymes from hepatocytes
*↑alkaline phosphatase: reflects the partial cholestasis
*abnormal clotting tests reflect the impaired hepatocyte function.
Lab findings form cholestatic jaundice
*bilirubin in the urine (characteristic dark colouration); this occurs as the bilirubin is conjugated and thus water-soluble
*no urobilinogen in the urine; due to the obstruction, no bilirubin enters the bowel to be converted to urobilinogen
*↑canalicular enzymes: alkaline phosphatase and γ-Glutamyl Transferase (GT)
*↑liver enzymes ALT and AST;
Control of bile release into duodenum
Sphincter of oddi
CCK- gallbladder to contract, reduce tone of oddi and pancreatic secretions
CCK release stimulated bu fats and acid in duodenum
Small amount of contraction due to vagus
Aldosterone effect in colon
Na absorbed
Causing water absorption
Use of colonic flora
Fermentation of indigestible carbs- producing fatty acids used by mucosa
Degredation fo blurbing to uro and sterco
Synthesis of vit K, B12, thiamin and riboflavin
Enteroglucagon- released by and function
Released in response to glucose and dat in ileum and colon
Inhibits gastric and small bowel motility
Use of copper and zinc
Copper- Synthesis of Hb and coenzyme in electron transport chain
Zinc- cofactor, synthesis of RNA, DNA
Vitamin deficiencies
A- night blindness
D- rickets, osteomalacia
E- haemorrhage anaemia
K- clotting
B1-thiamine- beriberi
2- riboflavin- dermatitis
3- pellagra- dermatitis, diarrhoea, dementia
6- convulsions, anaemia, skin lesions- pyridoxine
9- folate- anaemia
B12- cobalamin- anaemia
C- scurvy
Renal circulation
Renal artery- branches to interlobar artery between pyramids- form acuate- form interlobular - form afferent arterioles
Efferent arterioles -either form peritubular capillaries to renal tubules
Or descend as vasa recta- to medulla
When does auto regulation of kidneys fail
Systolic <80
Which hormones cause vasodilation of renal blood flow
Prostaglandin
NO
Which hormones cause vasoconstriction of renal blood flow
Angiotenin 1+2
Noradrenaline
Adrenaline
Features of endothelium and epithelium of Bowmans capsule allowing filtraitin
Ednothelium- fenestrated
Glycoproteins negative charge in BM- greater permeability of positive/neutral more than negative
Podocytes- do not form continuous layer
Forces in Bowman capsule generating urine
Hydrostatic pressure- greater than normal capillaries of 50mmg
Since proteins not filtered- opposing osmotic pressure of 10
Net 40
Area in kidney most prone to ischaemia
PCT as many ATP dependent pumps
Descending loop is permeable to
NaCl and water
But due to high osmolality surrounding- water moves out
Juxtaglomerular apparatus constituents and functions
JXG cells- specialised smooth muscle cells in afferent arteriole- secrete renin
- responds to decrease afferent pressure, stimulation by sympathetic nerves and macula densa
Macula densa- DCT- responded to reduction of Na
Where is Ca and P absorbed and regulated in kidneys
Actively absorbed in PCT
Remaining in DCT
Regulation by PTH in DCT
Management of acid base balance in kidneys
Majority of HCO3 absorbed in PCT
HCO3 +H is formed in tubular epithelium by CA after absorption of H2O and CO2
HCO3 absorbed and H+ secreted into lumen
Urea absorption in kidneys
Waste product not actively reabsorbed
But as water moves out- conc increases so small is passively reabsorbed
Criteria for substance to measure GFR
*must be filtered by the glomerulus
*must not be reabsorbed
*must not be secreted
*must not be metabolized
Nervous control of micturition
Para- sacral outflow S2-4- innervate bladder, internal sphincter. Also run in pudendal nerve and control external sphincter
Symp- L1-2 -hypogastric plexus - inhibit detrusor and increase contraction of internal
Bladder abnormalities from spinal cord injury
Reflex/autonomous Bladder – Spinal Cord Transection Above T12
In this case, the afferent signals from the bladder wall are unable to reach the brain, and the patient will have no awareness of bladder filling. There is also no descending control over the external urethral sphincter, and it is constantly relaxed.
There is a functioning spinal reflex-the bladder automatically empties as it fills – known as the reflex bladder.
Flaccid/atonic Bladder – Spinal Cord Transection Below T12
A spinal cord transection at this level will have damaged the parasympathetic outflow to the bladder. The detrusor muscle will be paralysed, unable to contract. The spinal reflex does not function.
In this scenario, the bladder will fill uncontrollably, becoming abnormally distended until overflow incontinence occurs.
Hypothalamus location
Forebrain
Floor of third ventricle
Pituitary gland tissue origin
Anterior- ectoderm in oral cavity - linked to hypothalamus via hypophyseal portal system
Posterior- continuous with hypothalamus
Causes of SIADH
*tumours, e.g. lung, pancreas, lymphomas
*TB
*lung abscess
*CNS lesions, e.g. meningitis, abscess, head injury
*metabolic, e.g. alcohol withdrawal
*drugs, e.g. carbamazepine.
Synthesis of thyroid hormones
*active pumping of iodide ions in from the extracellular space to the follicular epithelium
*iodide ions enter the colloid and are converted to iodine by TPO
*iodine is combined with tyrosine.
*Two forms are produced: monoiodotyrosine (1 MT) and diiodotyrosine (2 DT); these then combine to form the two thyroid hormones:
*triiodothyronine (T3): MT + DT
*thyroxine (T4): × 2 DT.
*More T4 is produced but T3 is more biologically active.
*Thyroid hormones are stored in the colloid of the follicle and released into the circulation as needed (the thyroglobulin is detached).
How thyroid hormones cause effect
T3 and T4 cross the cell membrane via diffusion; most of the T4 is converted to T3 in the cell.
*Thyroid hormone then bonds to nuclear receptors and initiates increased DNA transcription and protein production.
MOA of thioamides
Competitively inhibit TPO
Block coupling of iodotyrosine
PTU_ inhibits deionisation fo T4
Effects fo thyroid hormones
Metabolic- increased
Increased catabolism of FA and protein
Increased absorption of glucose
Increase HR, PVR, CO
Increased GI motility
Cause of secondary hyperthyroidism
Very rare
Pituitary tumour
Metastatic thyroid- well differentiated
Choriocarcinoma- usually HCG but can produce susbstances similar to TSH
Ovarian teratoma
Lab results of sick euthyroid
TSH and T3/4 can both be abnormally low
Cause of hypoparathyroidism
*congenital, e.g. DiGeorge syndrome
*autoimmune
*iatrogenic: following total thyroidectomy or parathyroidectomy
*hypomagnesaemia: low magnesium levels prevent the release of PTH.
Cause of vit D def
*dietary insufficiency: particularly common in vegans
*lack of sunlight: common in elderly patients and Asian women
*malabsorption: particularly after gastric surgery, coeliac disease and disorders of bile salt production
*renal disease: leads to inadequate conversion to the active form 1,25-dihydroxycholecalciferol
*hepatic failure
*Vitamin-D-resistant rickets: a familial condition with hypophosphataemia, phosphaturia and rickets.
Hypophosphataemia symptoms
*confusion
*convulsions
*muscle weakness: acute hypophosphataemia can lead to significant diaphragmatic weakness and delay weaning from a ventilator in patients in the intensive treatment unit
*left shift of oxyhaemoglobin curve: this results in decreased oxygen delivery to tissues and is due to the reduction in 2,3-DPG.
Release of hormones in adrenal medulla
Nerve fibres from the splanchnic nerves innervate the medulla; these release acetylcholine, which stimulates hormone release.
- pre ganglionic - Ach
*The chromaffin cells release a variety of hormones when stimulated to do so; they are stored in granules and exit the cells into the circulation via exocytosis.
*The adrenal medulla produces:
*epinephrine (adrenaline)- made from tyrosine
*norepinephrine (noradrenaline)
*dopamine
*β-hydroxylase (enzyme involved in catecholamine synthesis)
*ATP
*opioid peptides (metenkephalin and leuenkephalin).
Synthesis of steroids in adrenals
Cholesterol is converted to pregnenolone in mitochondria
Can go to progesterone- corticosterone- aldosterone
Or to progesteroneto 17a progesterone- cortisol
Or 17progester to Testosterone via 20 then to- oestradiol
What is cortisol bound to in the blood
Transcortin 75%
Albumin 15%
Rest active or free
Cortisol secretions is stimulated by
ACTH
Circadian rhymth- highest in the morning
*stress
*trauma
*burns
*infection
*exercise
*hypoglycaemia.
Effects of cortisol
Metabolic- opposite to insulin- breakdown of protein, converted to glucose- stored as glycogen
Lipolysis
Euphoria
Anti-inflammatory - synthesis of lipocortin- inhibits phospholipase A2
Secondary hyperaldosteronism causes
*renal artery stenosis
*congestive cardiac failure
*cirrhosis.
Effects of excess aldosterone secretion
*Na+ and water retention, leading to ↑ blood pressure
*renal K+ loss, leading to hypokalaemia
*renal H+ loss, leading to metabolic alkalosis.
congenital adrenal hyperplasia (CAH) most common cause and symptoms
The commonest defect affects the enzyme 21-hydroxylase.
decrease in cortisol secretion and as a result increases in ACTH secretion; this has the effect of driving the unused cortisol precursors into the androgenic hormone synthetic pathways.
*The clinical effects depend on the sex of the affected individual:
*male: there is rapid growth in childhood and early sexual development (precocious puberty); due to early fusion of the epiphysis, these patients are often shorter than average
*female: there is masculinization of the external genitalia with hypertrophy of the clitoris, a male body shape and hair distribution.
Gigantism vs acromegaly
Gigantism- childhood- before epiphyseal fusion
Acromegaly- after
GH metabolic effects
*↑glycogenolysis
*↓glucose uptake by cells
*promotes amino acid uptake into cells
*promotes protein synthesis
*↑lipolysis and release of free fatty acids (FFAs)
*↓LDL cholesterol.
Sx of acromegaly
Prominent supra orbital ridges
Visual defects
Broad nose
Heart failure
High BP
Galactohoea
Carpal tunnel
Insulin metabolic effects
Anabolic hormones
Promotes glucose uptake - except brain
Glycogen storage
Amino acid uptake
Protein synthesis
Inhibits lipolysis
Stimulates lipogenesis
Stimulants of somatostatin
*↑ plasma glucose
*↑ plasma amino acids
*↑ plasma glycerol.
Glucagon metabolic effects
Catabolic hormones
Increase glycogenolysis
Gluconeogenesis
Lipase- to increase FFA and glycerol
Effects of somatostatin
*inhibits the release of insulin and glucagons
*↓ gastrointestinal motility, secretion and absorption.
Other hormones effects on glucose regulation
GC-hypo- anti insulin
Promote lipolysis, gluconeo, glycogen
GH- fasting
Anti inuslin
Promote lipolysis, glucogenolysis
TH- low conc- anabolic
High- catabolic- hyperglycaemia
Catecholamines- when hypo
Glycogenolysis
Lipolysis
Secondary Diabetes mellitus causes
pancreatic disease:
*pancreatitis
*pancreatic cancer
*pancreatectomy
*cystic fibrosis
antagonists to insulin:
*acromegaly (GH)
*Cushing’s syndrome (glucocorticoids)
*hyperthyroidism (thyroid hormone)
*phaeochromocytoma (catecholamines)
*glucagonoma (glucagon)
*drugs, e.g. corticosteroids, thiazide diuretics
*liver disease
*genetic syndromes, e.g. Down’s syndrome, Friedreich’s ataxia
*insulin receptor abnormalities, e.g. congenital lipodystrophy
Pancreatic endocrine tumours
Insulinoma- B cell- whiles triad - 10% malignant
Gastrinoma- G cells- Malignant >50%
VIPoma- watery diarrhoea, low K, achlorhydria
Glucagonoma- a cell- 75% malignant- secondary diabetes mellitus; other symptoms include anaemia, weight loss and a characteristic rash called necrolytic migratory erythema
Somatostatinoma- d cells- diabetes, cholethiasis, steatorrhoea
Metabolic changes following surgery
divided into two phases: the ebb phase and the flow phase:
*the ebb phase is the initial response to injury and is a phase of reduced energy expenditure and metabolic rate that lasts for approximately 24h
*the flow phase follows: this is a catabolic phase with increased metabolic rate, hyperglycaemia, negative nitrogen balance and increased O2 consumption. The flow phase has significant effects on the metabolism of carbohydrates, lipids and proteins:
*carbohydrates: hyperglycaemia- this is stimulated by catecholamines and glucocorticoids (insulin resistance prevents cell uptake). After 24h the glycogen is exhausted and the hyperglycaemia is maintained by gluconeogenesis
*lipids: lipolysis is stimulated by catecholamines, the sympathetic nervous system, cortisol and growth hormone.
*proteins: the demand for amino acids is met by skeletal muscle breakdown; the greater the insult, the greater the breakdown and nitrogen loss. The amino acids are used in gluconeogenesis and synthesis of acute phase proteins.
Clinical changes post surgery
-hypovolaemia: this type of fluid loss is referred to as ‘third space’ loss; the vasodilatation and increased vascular permeability lead to fluid being sequestered in the interstitial space
*renal changes: following injury there is reduced excretion of free water and sodium; this continues for about 24h and is due to the release of aldosterone and ADH
*fever: injury (even in the absence of infection) is associated with a rise in temperature; this is due to changes in the thermoregulatory set point in the hypothalamus by IL-1
*haematological changes: there is a leukocytosis; albumin levels fall due to decreased production and loss into injured tissue. The coagulation system is activated. This is primarily to reduce bleeding after the injury; however, it leads to a state of hypercoagulability and an increased risk of deep vein thrombosis (DVT)
*electrolyte and acid–base changes: the electrolyte changes include ↓Na+ (due to dilution from retained water), ↑K+ (as a result of cell death and tissue injury), metabolic alkalosis (the absorption of Na+ stimulated by aldosterone leads to K+ and H+ excretion) and metabolic acidosis (this occurs with more severe injuries with hypotension, poor perfusion and consequent anaerobic metabolism).
-hyperglycaemia, lipolysis, ketones - form sympathetic innervation
- increased resp drive - resp alkalosis
- CO increases
Insulin post surgery
Low in ebb phase
Increase in flow phase- but hyperglycaemia due to resistance
Types of neurglial cells and function
Astrocytes- form BBB
Microglia- phagocytose
Oligodendrolgia- myelin in CNS
Autoregulation of cerebral blood flow
Occurs between 60-160mmHg
Myogenic - When the blood pressure rises, the vessels constrict, thus decreasing flow; when the blood pressure falls, the cerebral vessels dilate in order to increase flow.
Metabolic- increased activity results in a decrease in PaO2 and increase in PaCO2 and H+, the changes resulting in local vasodilatation of cerebral blood vessels and thus increased perfusion.
Neural- some sympathetic vasoconstrictor and parasympathetic vasodilator innervation, but their effect is very weak
Local- Increases in PaCO2 are associated with an increase in CBF due to marked cerebral vasodilatation; however, just as hypercapnia results in vasodilatation, then a fall in PaCO2 (hypocapnia) results in cerebral vasoconstriction.
The effect of changes in PaO2 is not as marked; hypoxia has a significant effect only when it falls below 8 kPa.
Increases in PaO2 can cause mild cerebral vasoconstriction; indeed hyperbaric oxygen therapy can reduce CBF by 20–30%.
Calculating CPP
DBP+1/3(systolic-diastolic) -ICP
CSF function
Hydraulic cushion
Stable ionic environment
Where CSF is reabsorbed
Arachnoid villi- which drain into venous sinuses
Features of BBB
Lipid soluble molecules can pass freely
Rather than the freely permeable fenestrated capillaries found in other tissues, the cerebral capillaries have very tight cell-to-cell junctions in the endothelium. In addition, the end-feet of astrocytes cover the basement membrane.
the endothelium contains transport proteins (carriers) for nutrients such as sugars and amino acids
*certain proteins, e.g. insulin and albumin, may be transported by endocytosis and transcytosis
Areas of BBB with fenestrated capillaries
third and fourth ventricles: allow drugs and noxious chemicals to trigger the chemoreceptor area in the floor of the fourth ventricle; this in turn triggers the vomiting centre. In addition angiotensin II passes to the vasomotor centre in this region to increase sympathetic outflow and causes vasoconstriction of peripheral vessels
*posterior lobe of pituitary: allows the release of oxytocin and antidiuretic hormone (ADH) into the circulation
*hypothalamus: this allows the release of releasing or inhibitory hormones into the portal–hypophyseal tract.
Brainstem death tests
7 areas- all must be absent
1.No pupillary response to light, direct or consensual: this reflex involves cranial nerves II and III.
2.Absent corneal reflex – normally would result in blinking; this reflex involves cranial nerves V and VII.
3.No motor response in the cranial nerve distribution to stimuli in any somatic area, e.g. supraorbital or nailbed pressure leading to a grimace.
4.No gag reflex: back of the throat is stimulated with a catheter; this reflex tests cranial nerves IX and X.
5.No cough reflex: no response to bronchial stimulation with a suction catheter; this reflex tests cranial nerves IX and X.
6.No vestibulo-ocular reflex: head is flexed to 30° and 50mL of ice-cold water is injected over 1min into each external auditory meatus; there should be no eye movements; this reflex tests cranial nerves III, VI and VIII.
7.Apnoea test: the patient is preoxygenated with 100% O2 for 10min; PaCO2 is allowed to rise to 5 kPa (before testing); the patient is disconnected from the ventilator and O2 is insufflated at 6L/min; PaCO2 is allowed to rise to 6.5 kPa; there should be NO respiratory effort.
Consequences of SOL
Raised ICP
Incracranial shift and herniation
Hydrocephalus- as will interrupt CSF flow
Site specific brain herniation
*transtentorial: the lesion lies within one hemisphere; leads to herniation of the medial part of the temporal lobe over the tentorium cerebelli (uncal)
*tonsillar: caused by a lesion in the posterior fossa; the lowest part of the cerebellum pushes down into the foramen magnum and compresses the medulla
*subfalcial: caused by a lesion in one hemisphere; leads to the herniation of the cingulate gyrus under the falx cerebri
*diencephalic: generalized brain swelling; leads to the midbrain herniating through the tentorium; this is termed coning
Systemic and clinical effects of raised ICP
*Cushing’s response: ↓ respiratory rate, bradycardia and hypertension
*neurogenic pulmonary oedema
*Cushing’s ulcers
*preterminal events include bilateral pupil constriction followed by dilation, tachycardia, ↓ respiratory rate, and hypotension.
*headache
*nausea and vomiting
*papilloedema
*decreased conscious level.
Clinical manifestation of transtentorial hernia
*oculomotor nerve compression: ipsilateral pupil dilation (transtentorial)
*cerebral peduncles: contralateral hemiparesis (transtentorial)
*posterior cerebral artery: cortical blindness (transtentorial)
*cerebral aqueduct: hydrocephalus (transtentorial)
Which hernia can cause compression in medulla resulting in death
Tonsillar
All can cause compression of midbrain resulting in death
Changes in Na and K as action potential starts
The Na+ channel activates much faster than the K+ channel. This explains the rapid influx of Na+; the channel also closes much faster; the K+ channel remains open over a longer period than the Na+ channel and is responsible for repolarization as K+ is released and the membrane potential falls back to its negative value.
Membrane potential valve
Resting -70mv
Depolarised- +50
Determinants of conductions velocity
Axon diameter
Myelination
Where are action potentials generated between myelin
Nodes of Ranvier
Causes AP to jump- saltatory conduction
Types of nerve fibre, function, speed and diameter
Aα Motor proprioception 100m/s 15–20um
Aβ Touch and pressure 50 5–10
Aγ Muscle spindles 30 3–6
Aδ Pain, temperature and touch 20 2–5
B Autonomic 10 3
C Pain 1 0.5–1
Synaptic transmission
*the action potential depolarizes the presynaptic membrane by opening voltage-gated Ca2+ channels
*Ca2+ enters the axon down an electrochemical and concentration gradient
*the increase in Ca2+ results in the vesicles fusing with the presynaptic membrane and releasing neurotransmitters into the synaptic cleft
*the neurotransmitters then bind with receptors on the post-synaptic membrane
*binding of neurotransmitters initiates secondary signals within the cell and opens ion channels, thus generating a depolarizing current
*the transmitter is released from the receptor and is broken down by specific breakdown pathways.
Types of neurotransmitters, function and what they are broken down by and into
Ach- excitatory - broken down to acetate and choline by acetylcholinesterase
*amines: this group includes catecholamines (adrenaline, noradrenaline, and dopamine), 5-hydroxytryptamine (serotonin) and histamine. The catecholamines are formed from the amino acid tyrosine. Two enzymes degrade catecholamines: monoamine oxidase breaks down transmitter taken up by the presynaptic neuron; and catechol-O-methyl transferase breaks down catecholamines taken up by the postsynaptic neuron
Amino acids: several amino acids act as neurotransmitters; these include:
*glycine: inhibitory
*glutamate: excitatory or inhibitory (can be converted to GABA)
*aspartate: excitatory
Peptides: examples of peptide transmitters include:
*substance P: involved in the transmission of pain sensation
*endorphins: inhibit pain pathways
Types of pain nerve fibres and function
*Aδ fibres: these are myelinated nerves; as a result, they have a high conduction speed and diameter. They are responsible for the sharp initial pain
*C fibres: these are unmyelinated nerves and thus have a smaller diameter and lower conduction velocity. They are responsible for the longer-lasting dull pain.
here they synapse in lamina I and III in the dorsal horn.
Pain transmission
Transduction- involves the production of electrical impulses; following tissue damage there is the release of inflammatory substances, i.e. prostaglandins, histamine, serotonin, bradykinin and substance P.
Transmission- pain sensation is along Aδ and C fibres to the spinal cord; here they synapse in lamina I and III in the dorsal horn.
Modulation of pain involves the ‘gate control theory’- These include inhibitory inputs from the periaqueductal grey matter and nucleus raphe magnus (both releasing serotonin) and the locus coeruleus (releases noradrenaline). In addition there is the release of the naturally occurring enkephalins and endorphins.
Connections and location of sympathetic NS
Pre- found in- in the thoracic and upper 2–3 lumbar segments of the spinal cord
*preganglionic neurons lie in the lateral horn of the spinal grey matter
*preganglionic axons leave via the ventral root of the spine to join the spinal nerve
*post-ganglionic neurons have their cell bodies either in the sympathetic chain or in a named plexus along the aorta, i.e. coeliac, superior and inferior mesenteric.
*Spinal nerves are connected to the sympathetic chain by two small branches: the lateral white ramus communicantes (myelinated), and the medial grey ramus communicantes (unmyelinated).
*The sympathetic innervation of the head and neck is via preganglionic neurons synapsing with post-ganglionic bodies within the sympathetic chain; the post-ganglionic neurons then leave via the grey rami communicantes to join the spinal nerve.
Difference in connections of head vs abdo SNS
*The sympathetic innervation of the abdominal and pelvic organs differs from that of the head and neck. Preganglionic neurons pass straight through the sympathetic chain to their individual plexuses and synapse with post-ganglionic cell bodies within the plexus.
Neurotransmitters of SNS
- Pre are Ach
*The neurotransmitter of the sympathetic nervous system is noradrenaline (except sweat glands; these are innervated by cholinergic fibres).
Pre ganglion of PNS vs SNS
PNS pre ganglion longer
Cell bodies of post ganglion- lie closer to organ
Composition of sarcomere
*the dark bands or A bands are composed of the thicker myosin filaments
*the light bands or I bands are composed of the thinner actin filaments
*the I band is divided by the Z line; the space between Z lines is called a sarcomere
*at the Z lines the membrane of the muscle cell (sarcolemma) forms narrow tubes that traverse the sarcomere; these are called the T-tubules
Actin filament proteins
*actin: a thin contractile protein, arranged in a double-stranded helix
*tropomyosin: lies in the groove between the actin filaments
*troponin: lies at regular intervals along the filament, attached to both actin and tropomyosin; it also has binding sites for Ca2+ and is involved in the regulation of contraction. Troponin and tropomyosin block the myosin-binding site on actin.
Types of skeletal muscle and properties
*type I or slow twitch: act as postural muscles, e.g. in the back; they are designed to perform slow, sustained contractions and resist fatigue well. They rely on aerobic metabolism and contain myoglobin
*type II or fast twitch:
*type IIa or fast oxidative fibres, e.g. calf muscles: they rely on aerobic metabolism and contain myoglobin; they have moderate resistance to fatigue
*type IIb or fast glycolytic fibres, e.g. extraocular muscle: do not contain myoglobin and thus appear white; they contain a large amount of glycogen and rely on anaerobic metabolism.
Sliding filament hypothesis
*When ATP binds to the head section of myosin it dissociates from its binding site on the actin filament.
*The ATP is hydrolysed (by ATPase on head) and changes the angle of the myosin head (relative to its tail); as the ATP has been hydrolysed, the myosin is again able to bind to the actin filament.
*The release of phosphate from the myosin head restores the angle and moves the actin filament along the myosin filament; this is called the power stroke.
*ATP will bind to myosin and start the process again.
*Creatine phosphate is present in very high concentrations within muscle and provides sufficient energy reserves for the above processes to take place. The enzyme creatine kinase catalyses the transfer of the phosphate group from creatine phosphate to ADP, thus replenishing ATP stores.
How Ca causes muscle contraction
Depolarization of the cell leads to the release of Ca2+ from the sarcoplasmic reticulum within the cell. The rise in Ca2+ activates contraction by binding to troponin on the thin filaments; this leads to a conformational change and removes troponin and tropomyosin from the myosin binding site on actin.
*As the cell repolarizes, the Ca2+ is actively pumped back into the sarcoplasmic reticulum.
*The Ca2+ is removed from the troponin and thus the troponin and tropomyosin block the myosin binding site.
Muscle reflex pathway
*muscle spindle is stretched: this causes the receptor region to depolarize; this generates an action potential in the afferent nerve (Ia afferent)
*the afferent impulse enters the spinal cord via the dorsal horn and synapses with an α motor neuron that supplies the stretched muscle
*the action potential in the α motor neuron signals the muscle to contract to oppose the stretch
*the afferent impulse also synapses with inhibitory neurons that synapse with α motor neurons that supply antagonist muscles (reciprocal inhibition). This reduces resistance to contraction of the stretched muscle.
Gamma reflex
After stretch
Intrafusal muscle fibres stretched- 1a efferent then type 2 slower- to provide proprioception info - causing a motor to contract
Gamma neurons to cause contractions of these fibres - causing stretching of mid portion that doesn’t have contractility- opening stretch Na channels- increasing resting potential- increasing likelihood of AP
Golgi Tendon Organ Reflex
The reflex they are involved in is an inhibitory response. It involves:
*afferent impulse 1b - acting on interneuron- via glutamine
Interneuron via glycine acts on α motor neurons that supply the contracting muscle
*reduction in the level of active contraction
*the reflex is protective and limits muscle/tendon tension
Withdrawal reflex
- withdrawal to painful stimulant- detected by cutaneous afferent neuron
*α motor neurons: this results in stimulation of flexors in the limb in which the painful stimulus was experienced, thus withdrawing the affected limb
*inhibitory signals are passed to α motor neurons in the opposing extensor muscles
*this pattern is reversed in the opposing limb: flexor muscles are inhibited and extensor muscles are stimulated; this is called the crossed extensor reflex
Descending motor pathways
*corticobulbar tracts: supply the motor portions of the cranial nerves
*corticospinal tracts: supply the spinal motor neurons; they are concerned with voluntary movements.
4 descending inputs from brainstem
Extrapyrimidal- involuntary control
1.The rubrospinal tract: originates in the red nucleus- cross over and primarily innervates distal limb muscles.- fine control in hands
2.The tectospinal tract: fibres arise in the superior colliculus of the midbrain; it receives inputs from the visual cortex and is believed to control reflex activity in response to visual stimuli.
3.The vestibulospinal tract: originates in the vestibular nuclei; it supplies muscles of the ipsilateral side of the body. It innervates muscles concerned with balance and posture in response to inputs from the vestibular apparatus.
4.The reticulospinal tract: fibres -The medial reticulospinal tract arises from the pons. It facilitates voluntary movements, and increases muscle tone.
The lateral reticulospinal tract arises from the medulla. It inhibits voluntary movements, and reduces muscle tone.
Metaraminol MOA
a1 agonsit
Used for acute hypotension
Which cells contribute the most to complement
Hepatocytes
Where are paneth cells found
Crypt of Lieberkuhn
Factors to increase flow rate
Short length, large diameter, low viscosity and high pressure
Renal blood flow following obstruction in first few hours
Initial increase due to prostaglandin and vasodilators
Then decrease due to vasoconstriction
Clearance calculation
U x V/P
urine conc x urine production /plasma conc
JVP waves and relations
a- atrial contraction just before carotid pulse
x- rapid atrial filling
c- ventricles begin to contract- bulge tricuspid back
v- atrial filling
y- opening of tricuspid
