Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MD1 > Physiology > Flashcards

Physiology Flashcards

1
Q

α1 adrenoceptor

A

Smooth muscle contraction

Rise in intracellular calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

α2 adrenoceptor

A

Prefrontal cortex cognitive function increase

Smooth muscle mixed effects

Cardiac relaxation

Platelet activation

intracellular cAMP decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

β1 adrenoceptor

A

Heart

AGONIST: increase cAMP
increase HR
increase contraction (increase SV)
increased lipolysis in adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

β2 adrenoceptor

A

Smooth muscle relaxation (bronchi & vascular dilator)

AGONIST:
increase cAMP
Smooth muscle relaxation
bronchodilation
vasodilation
increase liver glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clearance

A

Clearance = [ (drug conc in – drug conc out) / drug conc in ] * blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Renal Clearance

A

CLrenal = GFR + TS - TR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GFR

A

120mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Maximal CLrenal

A

800mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Coagulation

A

Initiation (TF exposed)
Amplification (prothrombin -> thrombiin = platelet activation)
Propagation (thrombin burst and fibrin clot formation)

Fibrinogen -(thrombin)-> fibrin = clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type I Respiratory Failure

A

Gas Exchange Abnormality
Decrease Pa02 < 60
Ventilation Increases
Decrease in PaCO2

(Hypoxaemia without Hypercapnia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Type II Respiratory Failure

A

Inadequate ventilation (by any cause)
Ventilation Decrease
Decrease Pa02
Increase PaCO2

(Hypoxaemia with Hypercapnia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Normal body temperature

A

36 - 37.5 degrees
+0.6 degrees in the afternoon
+1 degree post-ovulation

Oral Temp < core body temp by 0.5deg
Axillary temp < core body temp by 1deg

fever = increase in set point induced by pyrogens
PGE2 synthesis in hypothalamus (inhibited by aspirin)

PUO - fever above 38.3 for 2-3 weeks with know known cause

Optimal temp for immune response is 39.5deg

Rigors - feeling intense cold, shivering, pallor (vasoconstriction), exhaustion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pulmonary Artery Pressure

A

20-30mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

End Systolic Volume

A

75mL (reserve - can go up/down if needed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

End Diastolic Pressure

A

15mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Early Diastolic Pressure

A

5mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Heart sounds

A
  1. AV valve closure (tricuspid/mitral)
  2. Semilunar valve closure (aorta/pulmonary)
  3. Occurs at begining of diastole - oscillation of blood back and forth between the walls of the ventricles initiated by the inflow of blood from the atria
  4. Blood being forced into stiff hypertrophic ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Veinous Pressure

A

1 to 5 mmHg inside great veins (IVC/SVC)

7mmHg mean circulatory filling pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

O2 / CO2 metabolic requirements

A

REST
use 250ml/min O2
produce 200ml/min CO2

EXERCISE
use > 4000ml/min 02
produce > 4000ml/min CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Alveolar Volume & Surface Area

A

Volume
3-6 L

Surface Area
50 - 100 sqm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ficks Law (rate of diffusion of a gas)

A

V = A . D . (P1 - P2) / T

A = area
P1-P2 = difference in partial pressure
T = Thickness
D = diffusion rate (CO2 is 20x O2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Partial Pressures of O2 and CO2

  • inspired
  • alveoli
  • pulmonary artery
  • pulmonary vein
A

Inspired
O2 = 150 (20% composition of air)
CO2 = 0

Alveoli
O2 = 100
CO2 = 40

Artery
O2 = 98
CO2 = 40

Vein
O2 = 40
CO2 = 46

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q 
Lung Volumes
TLC
RV
VC
TV
FRC
FEV1
A

Total Lung Capacity - volume in lungs at full inspiration (5,700ml)

Residual Volume - volume in lungs at full expiration (1,200ml)

Vital Capacity - volume exhaled from TLC to RV (4,500ml)

Tidal Volume - volume of regular breath (500ml)

Functional Residual Capacity - volume remaining after regular breath (2200ml)

Forced Expiratory Volume 1 second (approx 70-80% of FVC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

A-a Gradient for oxygen

A

Measure of overall efficiency of gas exchange across all A-C units

PAO2 = PiO2 - PACO2 / RQ
A-a = PA02 - PaO2

(Normal < 15-30)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Suprachiasmatic Nucleus

A 
SCN governs some circadian rhythms
Receives input from 
- rods, cones (light)
- intergeniculate leaflet (activity)
SCN projects to the Paraventricular Nucleus which connects with the pineal gland (secrete melatonin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Sleep Generation

A

Two ascending arousal systems

  • ORX
  • LC, TMN, Raphe

Inhibitions
VLPO (activated by ATP depletion of arousal systems)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Neural GI Control Reflex

A

Vago-vagal (moderates ENS)
- control swallowing
- regulate acid secretion in stomach
- coordinate stomach and duodenum contraction
Intestino-intestinal
- vagus / dorsal root ganglia
- GI -> sympathetic ganglia -> reflex inhibition proximally when distal regions are distended
CNS
- anticipation of cephalic digestive phase, mood, activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Phases of digestion #1 - up to pylorus

A

Cephalic
- GI control systems activated prior to digestion
- salivation, gastric acid, pepsin, relaxation of corpus and fundus (storage)
- Vagal (stimulates ENS)
ACh M3 on parietal (H+) and ECL (histamine -> parietal), D-cell (somatostatin) inhibition of ECL histamine
G-Cell (gastrin) -> activate parietal via CCKR, activate distal D-Cell (somatostatin)[and H+] inhibition of G Cell

Distension (vagal afferent to hypothalamic appetite centre), stimulates pepsin & acid

(STRONG!) Pacemaker (ICC) propogation from corpus to antrum - mashing

Antrum

  • reflex inhibition of acid secretion in corpus
  • fat floats to top (fundus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Phases of digestion #2 - duodenum onwards

A

Duodenum

  • vago-vagal inhibition of gastric emptying (H+, distension, aa)
  • D-cell (somatostatin) - via portal vein
  • vago-vagal brunners gland secretion (bicarb)
  • duodenal-pyloro-antral reflex close pylorus
  • aa & fat trigger release of CCK from I-cells
  • aa triger release of Secretin from S-cells

Retropulsion - towards pylorus
Segmentation (ICC)
Peristalsis

Fat empties stomach last giving surge of CCK (suppressing appetite substantially)

Colon
water absorption
fermentation produces acetate, butyrate, propionate, stimulating enteric reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Cholecystokinin

A

released from I cells in duodenum

  • excites vagal afferent neurons (vago-vagal reflex, reduce appetite)
  • exicites ENS (activate mixing)
  • causes gallbladder contraction -> bile secretion
  • causes digestive enzyme production by pancreas
  • promotes release of insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Secretin

A

released from S cells in duodenum
causes secretion of bicarbonate from pancreas
retroperistalsis brings bicarb up into duodenum (neutralizes H+, deactivates pepsin, allows gastric emptying)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

GI sensing

A 
Mechanic & Distension
- vagal afferents, spinal afferents, ENS
Taste
- EC cells release serotonin
- L Cells (sweet)
-- release glucagon like peptide 1&2 and pancreatic polypeptide Y (regulate appetite and insulin secretion)
Olfactory
- EC cells release serotonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

General Liver Activities

A 
Energy storage (glycogen, fat, iron, Vit A etc.)
Production of cellular fuels
Lipid metabolism
Production of plasma proteins and clotting factors
Metabolism of toxins and drugs
Modification of hormones
Production of bile acids
Excretion of bilirubin
Storage of iron and vitamins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Protein Digestion

A 
STOMACH:
pepsin (cheif cells)
pepsinogen I (acid regions)
pepsinogen II (pylorus)
hydrolysis of aromatic amino acid bonds (phe & tyr)
DUODENUM/JEJUNUM:
CCK stimulates release of pancreatic proteases
trypsinogen -(enterokinase)-> trypsin
chymotrypsin
elastase
carboxypeptidase A & B

BRUSH BORDER
aminopeptidases, carboxypeptidases break polypeptides to amino acids
di- tri- peptides transported directly into epithelial cells
free aminos carried by 7 different transporters (Na+, Cl-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Carbohydrate Digestion

A

MOUTH:
α-amylase hydrolyses 1:4α linkages

DUODENUM/JEJUNUM:
pancreatic α-amylase & salivary activated at low pH

BRUSH BORDER:
isomaltase breaks 1:6α linkages
sucrase, maltase single large glycoprotein in membrane activated by pancreatic proteases

ABSORPTION:
Glucose/Galactose & Na+ SLGT1 of epithelium & GLUT2 into interstitium
Fructose GLUT5 (down conc. gradient) & GLUT2 into interstitium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Fat Digestion

inc. fat soluble vitamins A, D, E, K

A

MOUTH:
lingual lipase

STOMACH:
gastric lipase

DUODENUM:
CCK causes pancreatic lipolytic enzyme release and gallbladder constriction
lipases
cholesterol esterase (break down cell membrane)
bile salts, lecithin, vigorous mixing - emulsify fat
micelles form

ABSORPTION
dissolve in membrane at tips of villi
Fatty acids reform triglycerides in SER
+ apolipoprotein glycosilation = chylomicrons

Short chain fatty acids produced in proximal colon by fermentation of dietary fibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q 
Development
Zygote
Morula
Blastomere
Blastocyst
Blastocoel
Trophoblast
Inner Cell Mass
A

ZYGOTE: single cell
BLASTOMERE: cell produced by cleaveage of the Zygote
MORULA: 16 cell stage (3days)
BLASTOCYST: 58 cell stage (4 days)
BLASTOCOEL: Cavity of Blastocyst
TROPHOBLAST: Outer membrane of blastocyst (forms placenta)
INNER CELL MASS: Cells in blastocyst beginning to specialise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Ectoderm Derivatives

A 
Dorsal root ganglia
Sympathetic and Parasympathetic ganglia
Enteric ganglia
Schwann Cells
Melanocytes
Dentine
Muscle, Cartilage, and bone of skull, jaws, face, and pharynx.

(also neural crest derivatives - between ectoderm/neural tube)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Endoderm Derivatives

A 
Epithelum of:
GI tract
Respiratory tract
Tonsils
Thyroid
Parathyroid
Thymus
Liver
Pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Mesoderm Derivatives

A

PARAXIAL MESODERM
Derims of skin
Axial skeleton
Axial and limb muscles

INTERMEDIATE MESODERM
Urogenital System, kidney

LARTERAL MESODERM
Ventrolateral body wall
Limb skeleton
Visceral Pleura, Peritoneum, Pericardium
Blood Vessels and Blood forming tissue
Heart
Wall of Gut and Respiratory Tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Somitomeres

A 
Swellings down length of paraxial mesoderm
Split into:
DERMOTOME: dermis of skin
MYOTOME: back muscles
SCLEROTOME: axial skeleton

Medial Myotome: intrinsic back muscles (extensors)
Lateral Myotome: limb muscles, muscles of ventrolateral body wall, intrinsic back muscles (flexors)
Medial Sclerotome: vertebral body, intervertebral disk, proximal rib
Lateral Sclerotome: vertebral arch, pedicle of vertebra, distal rib.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Allantois

A

Branch of hindgut

Gives rise to bladder and urogenital tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Proctodeum

Stomadeum

A

PROCTODEUM: thin barrier where anus forms
STOMADEUM: thin barrier where mouth forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Coelom

A

Forms body cavity around viscera

Somatic Mesoderm + Ectoderm = body wall

Splanchnic Mesoderm + Endoderm = visera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Kidney Development

A

Pronephros
Neprostomes (degenerates) & pronephrotic duct
Mesonephris duct (connects to testes) & tubules
Metanephros (kidney!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

NEAT

A

NonExercise Activity Thermogenesis
Fidgeting, Posture, etc.
Accounts for difference in fat storage (gain) correlated to overfeeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Mediators of Weight / Eating (Neural)

A 
Arcuate Nucleus (influences PHN + LN)
stimulatefood intake:
- neuropeptide Y
- AGRP
- CB1
inhibit food intake:
- Cocaine and Amphetamine Regulated Transcript (CART)
- POMC (Melanocyte Stimulating Hormone (MSH)

Paraventricular Hypothalamic Nucleus (inhibit food intake)

  • oxytocin
  • CRH

Lateral Hypothalamus (stimulate food intake)

  • orexin
  • MCH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Mediators of Weight / Eating (Peripheral)

A

Leptin (fat cells)

  • Synthesised in adipocytes in proportion to cell size (inhibit eating)
  • transported to brain by receptor in choroid plexus
  • acts on Arcuate Nucleus of hypothalamus

Insulin (beta cells of islet)

  • signals to brain about levels of bf
  • action on liver = increase hunger
  • action on brain = decrease hunger
  • insulin insensitivity of liver may increase

Nutrients
- glucose -> Acetyl-CoA -(MCD)-> Malonyl-CoA –| CPT1

CPT1 breaks down LCFA-CoA (long chain fatty acid)
LCFA-CoA inhibits food intake

Stimulators:
- Ghrelin (stomach)
Inhibitors:
- CCK (intestine)
- PYY (intestine/colon)
- PP (phi cells of islet)
- GLP-1 (L cells)
- Amylin (β cells)
- Adrenaline
- Leptin
- Insulin
- Oxyntomodulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Causes of weight Loss

A 
ENDOCRINE
- untreated Type I Diabetes
- thyrotoxicosis
- Addison's (cortisol lack)
GI
- pancreatitis
- CF
- IBD
- parasitic
INFECTION
- TB
- endocarditis
- amoebic abcess
- HIV
MALIGNANCY
- GI
- Lymphoma
- Leukemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Phase I Metabolism

A

Creates chemical functional group on drug
(e.g. -OH, -NH2, -SH, -COOH)

  • typically due to Cytochrome P450
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Phase II Metabolism

A

Conjugation of water soluble molecule to functional group on drug

  • e.g. glucuronyl transferase (add glucuronyl acid)
  • molecule typically becomes more water soluble
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Rapid IV administration

A 
dX/dT = -KX
X = Xo e^(-Kt)
logC = logCo - (K/2.303)t
t1/2 = 0.693/K
CL = KVd
X = amount of drug in body
K = elimination rate constant
C = plasma concentration

Cpeak ~ Xo / Vd

  • drug distributes rapidly and reaches equilibrium
  • behaves as if in single compartment
  • first order kinetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Short term I.V. infusion

A

dX/dT = ko -KX

  • drug infused at constant rate ko
  • rapid distribution
  • peak not as high as for i.v. bolus
  • first order kinetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Long term I.V. infusion

A 
Css = ko/(VdK)
Css = ko/CL

Css = steady state concentration

2x ko = 2x Css

Can be done through multiple dosing

  • dose every half life
  • gives two-fold variation in concentration (trough = peak/2)
  • most drugs have greater than two-fold therapeutic window
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Oral Administration

A

dX/dT =KaXa - KX

Ka = absorption rate constant
Xa = amount of drug at absorption site
  • first order elimination
  • peak not as high as with i.v. due to elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Drug Bioavailability

A

Proportion of active drug which enters systemic circulation

Area of C vs t curve

AUCoral / AUCiv %

Factors affecting bioavailability

  • route of administration (I.V. = 100%)
  • taken with food
  • interactions
  • drug properties (pKa, hydrophobicity, solubility)
  • first pass metabolism
  • disease states
  • enzyme induction/inhibition for activation/deactivation
  • age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Rapid IV administration of Slow Distributing Drugs

A

Problem if drug has small therapeutic window
Initial loading dose must be higher than if drug distrubuted rapidly (Cpeak high)
loading dose can be divided to avoid toxic Cpeak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Rapid IV administration of Zero Order Elimination

A

Elimination is saturated and occurs at constant rate
Multiple dosing never reaches steady state as elimination is not proportional to concentration

Increasing dose rate leads to disproportionate increase in concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Drug-drug interactions

  • Pharmacodynamic
  • Pharmacokinetic

(to be clinically important drug B must have narrow therapeutic index and have steep concentration response curve)

A

PHARMACODYNAMIC
Receptor antagonism (beta agonist/antagonists)
Physiological
Synergistic (co-trimoxazole)

PHARMACOKINETIC
Absorption 
- gastric emptying rate (e.g. opioids)
- formation of poorly absorbed complexes
Distribution
- displacement from plasma protein 
Metabolism
- induction/inhibition of cytochrome p450
Excretion
- protein binding and filtration
- inhibit tubular secretion (e.g. probenecid in sports)
- urine flow & pH (NaHCO3 in aspirin overdose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Renal Plasma Flow

A

600ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Kidney GFR maintenance mechanisms

A

Myogenic Reflex of afferent arteriole
Macula Densa detect NaCl and provide feedback via paracrine mediators (adenosine, prostaglandins)
Tubuloglomerula Feedback
Angiotensin II preferentially constricts efferent arteriole
Prostaglandins mediate afferent arteriole dilation
Renin release from JGA Granular Cells in afferent arteriole
- macula densa
- sympathetic
- contraction of afferent arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Forces/Pressures that affect GFR

A

Hydrostatic Pressure in Glomerular Capillary - 50mmHg
Hydrostatic Pressure in Bowman’s Capsule - 10mmHg
Oncotic Pressure in Glomerular Capillary - 25-40mmHg
Oncotic Pressure in Bowman’s Capsule - 0mmHg

Oncotic pressure due to impermeable proteins (basal lamina highly negatively charged)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

GFR Autoregulation Range

A

80mmHg - 180mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

RBF equation

Pressure equation

A

RBF = ΔP ÷ R

P = flow x R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Excretion vs Renal Clearance (equations)

A

Excretion = Urine Concentration * Urine Volume

Renal Clearance = Excretion / Plasma Concentration

clearance is defined as volume of plasma cleared of substance per time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Filtration, Reabsoption, Secretion of

Water & Na+

A 
Water & Na+ almost entirely reabsorbed
Occurs throughout entire nephron
Only final bit in collecting duct is regulated
Water - ADH (vasopressin)
Na+ - Aldosterone

0.5-1% EXCRETION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Filtration, Reabsoption, Secretion of

K+

A

K+ reabsorbed in proximal tubule and distal tubule (to an extent)
Undergoes net secretion in distal tubule and collecting duct

10% EXCRETION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Filtration, Reabsoption, Secretion of

Ca2+

A

Ca2+ almost entirely reabsorbed (primarily in proximal and distal tubule).
Under control of PTH proximal and Vit D3 distal (favoring Ca2+ retention)

2% EXCRETION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Filtration, Reabsoption, Secretion of

Phosphate

A

Phosphate mainly absorbed in proximal tubule (some distal)
Co-transport with Na+

20% EXCRETION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Filtration, Reabsoption, Secretion of

Glucose

A

Glucose and amino acids are 100% reabsorbed (if plasma concentration < 15mmol)
Reabsorption in proximal tubule co-transport with Na+

0% EXCRETION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Plasma creatinine & GFR

A

If creatinine in the blood is rising it tells you that GFR is falling
15% of plasma creatinine is bound to plasma proteins (understimates GFR)

100% EXCRETION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Reabsorption & Ion channels in Early Proximal Convoluted Tubule

A

APICAL

  • Glucose/AA,Na+ cotransport (in)
  • Na+ (in) / H+ (out)

BASOLATERAL

  • Glucose/AA channels (out)
  • Na+ / K+ ATPase
  • Na+ / HCO3- co-transport (out)

PARACELLULAR
Leak of Na+ into lumen (proximally), out (distally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Reabsportion & Ion channels in Late Proximal Straight Tubule

A

APICAL

  • HBase passive diffusion in
  • Na+ (in) / H+ (out)
  • Cl- (in) / Base- (out)

BASOLATERAL

  • Cl- channels (out)
  • Na+ / K+ ATPase
  • Cl- / K+ co-transport (out)

PARACELLULAR
Leak of Na+ out of lumen (into interstitium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Reabsportion & Ion channels in Thin Descending Limb

A

H20 passive diffusion (out)

Epithelium is thin but has little mitochondria (can’t pump effectively)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Reabsportion & Ion channels in Thin Ascending Limb

A

Na+ passive diffusion (out)

Due to concentration gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Reabsportion & Ion channels in Thick Ascending Limb

A

APICAL

  • Na+/K+/2Cl- co-transport (in) [Target for Frusemide]
  • K+ channel (out)
  • Na+ (in) /H+ (out)

BASOLATERAL

  • K+ & Cl- channels (out)
  • Na+ / K+ ATPase
  • Cl- (in) / HCO3- (out)

PARACELLULAR
Leak of Na+ out of lumen (into interstitium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Reabsportion & Ion channels in Distal Convoluted Tubule

A

APICAL
- Na+/Cl- co-transport (in) [Blocked by Thiazide Diuretics]

BASOLATERAL

  • Cl- channels (out)
  • Na+ / K+ ATPase

Thiazides not as effective as Frusemide because frusemide acts earlier (25% sodium absorbed in loop, <10% absorbed in DCT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Reabsportion & Ion channels in Collecting Tubule

A

APICAL

  • Na+ channel (in)
  • K+ channel (out)

BASOLATERAL

  • K+ channel (out)
  • Na+ / K+ ATPase

[Aldosterone]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Plasma Buffer Systems

A

Carbon Dioxide
CO2 + H2O H+ + HCO3-

Plasma Proteins
PPR– + H+ <> PPRH-

Phosphates
HPO4– + H+ H2PO4- + H+ H3PO4

Haemoglobin
Hb + H+ HbH+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Normal anion Gap

A

12mmol/L

This is mostly due to anions contributed to by plasma proteins which are largely negatively charged (80% albumin)

Na+, K+ add up to 150mmol/L
HCO3-, Cl- add up to 138mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Kidney Acid-Base Balance Mechanism

A

HCO3- reabsorption (100%) in proxmial tubule

HCO3- and Na+ Filtered
Na+/H+ pumps H+ into lumen
CA forms H2O and CO2 which diffuse into cell
CA forms H+ (excreted again) and HCO3-
Na+/HCO3- co-transport into interstitum

Glutamine metabolised to NH4+ and HCO3- (in cell)
NH4+/Na+ pumps NH4+ into lumen
Na+/HCO3- co-transport into interstitum

Response to Acidosis:
(In cell) CA forms H+ and HCO3-
HCO3- reabsorbed to buffer acidosis
H+ excreted into lumen and binds with HPO4– to form H2PO4-

Distal Tubule Intercalated Cell (type A)
HCO3- buffers H+ in interstitum to form CO2 and H2O
CO2 and H2O diffuse into cell
CA forms H+ (excreted again) and HCO3-
HCO3- and Cl- exchange basolateral
H+ exchanged with K+ apical
K+ absorbed basolateral
Distal Tubule Intercalated Cell (type B)
(In cell) CA forms H+ and HCO3-
HCO3- exchanged with Cl- apical
H+ exchanged with K+ basolateral
K+ diffuse out apical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Vesico-uretic Reflux

A

Failure to prevent urine flowing back up ureters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Neural Fold Closure Sequence

A
  1. Back
  2. Cranium - (Acromegaly - no structures above eyes)
  3. Face
  4. Occipital
  5. Sacral - (Spina Bifida - open neural tube - folate protective)
84
Q

Segmentation of Neural Tube

A
  1. Prosencephalon (forebrain)
    - Telencephalon (cortex, basal ganglia, hippocampus)
    - Diencephalon (inc. optic vesicles)
  2. Mesencephalon (midbrain)
  3. Rhombencephalon (hindbrain)
    - 7 segments
    - Metencephalon (pons/cerebellum)
    - Myelencephalon (medulla)
85
Q

Sonic Hedgehog

A

Released by notochord -> induces floor plate in neural tube

Released by floor plate -> induces ventral horn motor neurons

(motor neurons then release Motor Neuron Factor which induces interneurons)

86
Q

Dorsal Column Medial Lemniscus (mechanosensory)

A

Ascending pathway
Fine touch, Proprioceptoion, Vibration

Lower Mechanoreceptors travel in Gracile Tract (Medial) T7 and below
Upper Mechanoreceptors travel in Cuneate Tract (Lateral) T6 and above

Synapse with INTERNAL ARCUATE FIBRES in Caudal Medulla and cross over at MEDIAL LEMNISCUS (umr become medial)

Synapse in Ventral Posterior Lateral (VPL) nucleus of thalamus towards primary somatic sensory cortex

87
Q

Corticospinal Tract

A

Descending pathway
Controls motor function

Cortex
Internal Capsule
Cerebral peduncle
Travels in ventral brainstem
Crosses at pyramids (medulla\)
Travels postero-lateral in spinal cord
88
Q

Anterolateral System (Spinothalamic)

A

Ascending pathway
Pain, Temp, Crude Touch
Synapses then crosses in spinal cord (anterior white commissure)
Terminates at thalamus (VPN), midbrain, and reticular formation

89
Q

Tracts & function:

  1. Dorsal Column Medial Lemniscus System*
  2. Spinocerebellar
  3. Spinothalamic*
  4. Spino-olivary
  5. Extrapyramidal Tracts
  6. Pyramidal Tracts*
A

ASCENDING

1a. Gracile - LL - fine touch, proprioception
1b. Cuneate - UL - fine touch, proprioception
2a. Posterior - proprioceptrion from muscle spindle and golgi
2b. Anterior - proprioception from golgi
3a. Lateral - pain/temp
3b. Anterior - crude touch / pressure
4. N/A - proprioceptive

DESCENDING

5a. Vestibulospinal - balance, posture (from vestibular nuclei)
5b. Olivospinal
5c. Reticulospinal - locomotion, posture (decerebrate posture) (from reticular formation)
5d. Rubrospinal - UL flexion (decorticate posture) (from red nucleus)
6a. Anterior Corticospinal - direct motor control (postural maintenance)(10-15% of fibres)
6b. Lateral Corticospinal - contralateral motor control (primary)

90
Q

Short v Long Propriospinal Tracts

A

SHORT:
lateral, ipsilateral
complex/dextrous movement
over small region

LONG
medial, bilateral
large movements (e.g. pelvic girdle)
large area

91
Q

UMNL vs LMNL

A 
UMNL (loss of inhibition)
increased tone
decreased power
increased reflexes
positive Babinski
LMNL (no activation)
decreased tone
decreased power
decreased reflex
no Babinski
92
Q

CSF & raised ICP

A

CPP = MAP - ICP

150mL each of blood and CSF

CAUSES:
Trauma
Tumour
Infection
Haemorrhage
Infarction
Oedema
- Vasogenic - BBB increased permeability (white matter affected) - steroids help
- Cytotoxic - increased intracellular fluid secondary to cell membrane injury (grey & white matter)
CSF disorders
93
Q

Brain Herniations

A

Subfalcine (cingulate gyrus)
Transtentorial (medial temporal lobe)
Transforaminal (cereballar tonsils)

94
Q

Pupillary Light Reflex

A

Sensory input from CNII
Melanopsin GC’s project to the Optical Pretectal Nucleus (OPN) in midbrain
Synapse bilaterally on Edinger Westfal Nucleus
Motor output to Ciliary Ganglion then Sphincter Pupillae muscle in iris via CNIII (parasympathetic)

95
Q

Corneal Blink Reflex

A

Sensory input to brainstem (ipsilateral pons) via CNV1
Bilateral motor output to eyelid (orbicularis oculi) by CNVII
(via IAM, facial canal, stylomastoid foramen, and parotid)

Used as test of Pontine function

96
Q

Gag Reflex

A

Sensory input: IX from pharynx (ipsilateral) to trigeminal nucleus
Interneurons to nucleus ambiguus (bilateral)
Motor output: X to pharynx

Used as test of Medulla function

97
Q

Types of Eye Movements

A

Saccadic - shift eye to new target

Smooth pursuits - following a moving object

Vergence - focusing on something coming closer

Vestibular-occular - hold image still during head movement

Optokinetic - e.g. sitting on a train looking out window

98
Q

Horizontal Eye Movement (Saccade)

A

(L) Frontal Eye Fields (prefrontal cortex) ->
(R) Paramedian Pontine Reticular Formation (PPRF) ->
(R) Burst&Omnipause Neurons ->
(L) Abducens nucleus inhibition & (R) Abducens nucleus activation ->
(R) Abducens causes (R) eye abduction
(R) Abducens projects via Medial Longitudinal Fasiculus to (L) CNIII nucleus ->
(L) CNIII nucleus innervates Medial Rectus

= Look to the right

  • Burst neuron: Fire at high frequency before movement
  • Omnipause: Fire continuously during movement
99
Q

Vestibular Occular Reflex

A

Turning Head Left

(L) CNVIII ->
(L) vestibular nuclei in medulla ->
inhibition of (L) CNVI nucleus, activation of (R) CNVI nucleus ->
(R) abducens actvivation
(R) CNVI nucleus projects via MLF to (L) CNIII and activates (L) Medial Rectus

Also a direct connection from (L) Vestibular Nucleus to (L) CNIII (Medial Rectus)

There is also inhibitory input from (R) CNVIII

100
Q

Colour Vision Deficiencies
Protanope/Protanomal
Deutanope/Deutanomal
Tritanope/Tritanomal

A

Protanope - no red cone
Protanomal - abnormal red cone

Deutanope - no green cone
Deutanomal - abnormal green cone

Tritanope - no blue cone
Tritanomal - abnormal blue cone

101
Q

Physiology of Breathing

A

INPUT:
Irritant receptors
stretch receptors
peripheral chemoreceptors (carotid & aortic bodies) - O2, pH, CO2
central chemoreceptors (ventral medulla) - pH

MEDULLA (nucleus solitarius)

OUTPUT:
phrenic nerve (diaphragm)
intercostal nerves (intercostals)
SCM (CNXI)

102
Q

Metabolic Acidosis

A

decreased pH
Normal CO2
Decreased HCO3-

103
Q

Metabolic Alkalosis

A

increased pH
Normal CO2
Increased HCO3-

104
Q

Respiratory Acidosis

A

decreased pH
increased CO2
Normal HCO3-

105
Q

Respiratory Alkalosis

A

increased pH
decreased CO2
Normal HCO3-

106
Q

Monosynaptic Reflex

A

muscle spindles in intrafusal fibres -> Ia sensory afferent -> ventral horn -> α-motor neuron -> extrafusal fibres -> contraction

γ-motor neurons keep intrafusal fibres taut

107
Q

Golgi tendon reflex

A

Prevent damage to contracted muscle by sensing increases in tension and causing relaxation

Golgi body senses tension -> inhibiting interneuron -> α-motor neuron inhibited -> relaxation

108
Q

Cochlear Hair Mechanism

A

K+ channels partially open
Displacement towards kinocilia -> opening of K+ channel -> depolarisation -> opening of Ca2+ channels -> glutamate release
Hyperpolarization in opposite direction (not as strong as depolarization)

109
Q

Auditory Pathway

A

Hair cells
CNVIII (spiral ganglion)
Cochlear Nucleus (medulla)
Superior Olive (work out where sound is coming from)
- Lateral (intensity), Medial(time), and Trapezoid body (contralateral inhibition)
Lateral Lemniscus
Inferior Colliculus
Medial Genticulate Nucleus (Thalamus)
Auditory Cortex (Temportal Lobe) - herschls gyrus

110
Q

Vomiting Mechanism

A 
Stimulants:
5-HT3
D2
H1&H2
Higher Centres

Chemoreceptor Trigger Zone (medulla oblongata - outside BBB) -> Solitary Nucleus / Vomiting Centre -> vomitting pattern generation

Retroperistalsis
Gastric Pyloric Contraction
Abdominal wall / thoracic contraction
epiglottis closure

111
Q

Swallowing Mechanism

A

Afferents: IX
Efferents: V, X, XII

Salivation (VII, IX)
Mastication (V, VII, XII)
Bolus shaped by tongue (XII)
Soft palate decends, palatal arches grip and push bolus to oropharynx (X)
Soft palate elevates (V, X)
larynx/pharynx elevated (X)
epiglottis/laryngeal inlet closed (X)
bolus pushed down oropharynx over epiglottis (X)
bolus forced down laryngopharynx to oesophegus (X)
larynx return to normal (elastic recoil)

112
Q

Pineal Gland

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Melatonin [AA]
Brain/other
Circadian Rhythm, immune function, antioxidant

113
Q

Hypothalamus

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Trophic Hormones* [P]
Anterior Pituitary
Release/inhibit pituitary hormones

* PRH -> Prolactin
PIH (Dopamine) -> Prolactin
TRH -> TSH
CRH -> ACTH
GHRH-> GH 
GHIH (somatostatin) -> GH (somatotropin)
GnRH -> LH & FSH
114
Q

Posterior Pituitary (neurohypophysis)

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Oxytocin [P]
Breast & Uterus
Milk ejection, labour, behaviour

Vasopressin (ADH) [P]
Kidney
Water reabsorption

115
Q

Anterior Pituitary (adrenohypophysis)

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Prolacin [P]
Breast
Milk production

Growth hormone (GH-somatotropin) [P]
Liver/other
Growth factor secretion (IGF-1), growth, metabolism
Hyperplasia, hypertrophy, increase protein synthesis, anti-insulin (increase blood glucose)
* more GH released in presence of Ghrelin!!

Corticoropin (ACTH) [P]
Adrenal Cortex
Cortisol, Aldosterone, & DHEA Release
Melanocortins & endorphins

Thyrotropin (TSH) [P]
Thyroid
Growth Hormone Synthesis

FSH/LH [P]
Gonads
Egg/Sperm production, sex hormone production

116
Q

Thyroid

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Triiodothyronine and thyroxine [AA]
Many Tissues
Increase BMR, O2 consumption, heat, growth, development, HR, CO
Cuboidal follicular cells surrounding GAG/TG mix

Calcitonin [P]
Bone
Plasma calcium levels (excrete & store calcium)
C-cells in interstitial spaces

117
Q

Parathyroid

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Parathyroid Hormone (PTH) [P]
Bone & Kidney
Increase Ca2+ plasma levels (and regulate Phosphate)
- increase [Ca2+] & [PO4] from bone
- increase [Ca2+] from kidney (proximal tubule) but decrease [PO4]
- indirectly (via Vit D) increase [Ca2+] & [PO4] from intestine
Essential for life

  • minutes - kidney transport
  • 1-2 hours - increased osteoclast activity (paracrine, not PTH directly)
  • 2-3 hours - bone reabsorption
  • 1-2 days - intestinal reabsorption

acutely PTH promotes osteoblast development and activity - favouring bone anabolism

118
Q

Thymus

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Thymosin, thymopoeitin [P]
Lymphocytes
Lymphocyte development

119
Q

Heart

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Atrial Natriuretic Peptide [P]
Kidneys
Increase Na+ excretion

120
Q

Liver

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Angiotensinogen [P]
Adrenal Cortex / Blood Vessels
Aldosterone secretion, increase BP

Insulin-like Growth Factors (IGF- somatomedins) [P]
Many tissues
Growth (bone, protein, antilipolytic)

121
Q

Stomach/GI

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Gastrin, Cholecystokinin, Secretin, others [P]
GI tract and pancreas
Assist Digestion and absorption of nutrients

122
Q

Pancreas

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Insulin, Glucagon, Somatostatin, Pancreatic Polypeptide [P]
Many Tissues
Metabolism of glucose and other nutrients

123
Q

Adrenal Cortex

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Aldosterone [S]
Kidney
Na+ and K+ homeostasis, BP

Cortisol [S]
Many Tissues
Stress Response (protein/carb/lipid metabolism, immune)

Androgens [S]
Many Tissues
Sex drive in females

124
Q

Adrenal Medulla

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Adrenaline, Noradrenaline [AA]
Many tissues
Fight or flight, increased glucagon, decreased insulin

125
Q

Kidney

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Erythropoeitin (EPO) [P]
Bone Marrow
RBC production

1,25 Dihyrdoxy-vitamin D3 (calciferol) [S]
Intestine
Increase calcium absorption

126
Q

Skin

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Vitamin D3 [S]
Intermediate form of hormone
Precursor to 1,25 Dihyrdoxy-vitamin D3 (calciferol)

127
Q

Testes

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Androgens [S]
Many tissues
Sperm production, secondary sex characteristics

Inhibin [P]
Anterior Pituitary
Inhibit FSH secretion

128
Q

Ovaries

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Estrogen, Progesterone [S]
Many Tissues
Egg production, secondary sex characteristics

Inhibin [P]
Anterior Pituitary
Inhibit FSH secretion

Relaxin (pregnancy) [P]
Uterine Muscles
Relaxtion of muscle

129
Q

Adipose Tissue

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Leptin, adiponectin, resisitin
Hypothalamus, other tissues
Food intake, metabolism, reproduction

130
Q

Placenta

  • Hormone(s)
  • Target(s)
  • Effect(s)
A

Estrogen, Progresterone [S]
Many Tissues
Fetal, maternal development

Chorionic somatomammotropin [P]
Many tissues
Metabolism

Chorionic gonadotropin [S]
Corpus Luteum
Hormone secretion

131
Q

Growth Hormone (somatotropin)

  • Stimulation
  • Action
A

GHRH + Ghrelin stimulate Anterior Pituitary to release GH (somatotropin)
GHIH (somatostatin) inhibit Anterior Pituitary

GH act on peripheral tissues
GH act on liver to produce IGF-1 (somatomedins)

GH binds to monomer of GHR, binds another at second binding site (lower affinity) forming active dimer and receptor activation
Glycine at amino acid position 120 is necessary for GH activity -> mutate and pegylate

132
Q

Cortisol

A

Released in response to ACTH on Adrenals (Zona Fasciculata)

  • Binds to transcortin in the blood
  • Stimulates protein breakdown to amino acids (Gluconeogenesis)
  • Inhibits protein synthesis
  • Increases blood glucose levels
  • Inhibits utilization of glucose by adipose tissue
  • Facilitates lipid breakdown to fatty acids (lipolysis)
  • Promotes lipid storage in abodomen, head, chest
  • Stimulates appetite and excessive eating (weight gain)
  • decreases Ca2++ absorption, increases excretion & bone breakdown
  • Suppresses immune responses by suppressing cytokine synthesis. I.e. elevates levels of IκBα which bind to NF-κB (induced by TNF-α)
  • Peaks in morning, low at night
  • inhibits childhood growth (but sick kids don’t grow either)

Cortisone -11βHSD1-> Cortisol
Cortisol -11βHSD2-> Cortisone

  • 11βHydroxysteroid dehydrogenase
133
Q

Progesterone

  • Signal
  • Secretion From
  • Function
A

LH

Corpus Luteum

Maintains (with estradiol) the uterine endometrium for iimplantation of fertilized oocyte

134
Q

17β- Estradiol

  • Signal
  • Secretion From
  • Function
A

FSH

Ovarian Follicle, Corpus Luteum, Sertoli Cell
(small amounts from adrenal cortex & testicles)

Females: regulates gonadotropin secretion in ovarian cycle, maintains uterine endometrium, growth of mammary gland.

Males: negative feedback inhibitor of Leydig cell synthesis of testosterone

135
Q

Effects of CRH

A

Release of ACTH by pituitary
Inhibits appetite
Signals onset of Labor

136
Q

POMC

A

Pro-opiomelanocortin
Large protein that yields several peptides by proteolysis
- ACTH = cortisol, aldosterone, sex hormone release
- β-endorphin = reduced pain sensation
- α & γ MSH = decreased appetite, increased melanin

137
Q

GLP-1 (Glucagon-Like Peptide 1)

A

Secreted from L Cells of small intestine
Released in response to glucose and fatty acids
Binds to specific receptor on pancreatic β-cells

Inhibits glucagon secretion
Stimulates insulin synthesis
Promotes β-cell proliferation
Promotes β-cell differentiation
Stimulates β-cell maturation
Decreases β-cell apoptosis 
Slows gastric emptying
Decreases appetite

Degraded by DPP-IV

Drug: Exenatide
Decreases BP and slightly increases HR
SITES: Nausea, diarrhoea, vomiting, abdo pain

138
Q

Ghrelin

A 
Secreted from stomach
Acts on hypothalamus
Increases appetite by increasing  synthesis / secretion of NPY
Fluctuates preceding each meal
Opposes leptin
139
Q

GIP

A

Released form K cells in duodenum and jejunum after digestion of food
Stimulates insulin release
Activates lipoprotein lipase (storage of fat)

140
Q

PYY

A

Made in L cells of distal GI (same as GLP-1)

Binds to Y2 receptor and reduces food intake

141
Q

CCK

A

Made in I cells of small intestine.
Has short half life.
Stimulates Gallbladder and pancreas.
Acts on vagus to reduce appetite.

142
Q

Oxyntomodulin

A

Product of glucagon gene.
Release from L-cells.
Reduces food intake, increases energy expenditure.
Acts on GLP-1 receptor and inactivated by DPP-IV. Slightly more potent than GLP-1.
Synergistic with PYY

143
Q

Uroguanilin

A

Produced in distal gut and acts on hypothalamus to decrease food intake.
Acts on gut to increase intestinal fluid absorption

144
Q

ILP-5

A

Predominantly expressed in colon and ileum.
Causes increase in food intake (not as powerful as ghrelin)
Modulated based on food intake (suppressed after eating)

145
Q

Bone

  • structure
  • growth
A

Hydroxyapatite (Ca10 (PO4)6 (OH)2) - calcium phosphate

Outer compact / cortical bone (haversian systems)
Inner trabecular / cancellous bone (lamellae)
Marrow (red in scapula, skull, jaw, pelvis) w/ porous sinusoids
Outer Periosteum (fibroblasts, vessels, collagen, osteoprogenitor cells)
Inner Endosteum (osteoprogenitor cells)

Arteries supply discrete sections (diaphyseal, epiphyseal, metaphyseal, seperate periosteal), w/ abundant nerves

Sharpey’s fibres - bone collagen continuous with tendon/ligament collagen

ENDOCHONDRAL GROWTH

  • cartilage model produced first (Type II)
  • bone collar forms around diaphysis
  • cartilage beneath degenerates
  • blood vessels invade w/ progenitors
  • from diaphysis at epiphyseal growth plate
  • chondrocyte columns continuously dividing and laying down collagen
  • secondary ossification centre at epiphysis
  • osteoblasts increase Ca2+ and PO-, causing precipitation

INTRAMEMBRANOUS GROWTH

  • forms directly from mesenchyme
  • skull, flatbones, mandible, clavicles
146
Q

Osteoblasts

A

Bone forming cells (modified fibroblasts)
From osteoprogenitor cells of periosteum & endosteum
Flat when quiescent
Look like plasma cells when active (perinuclear hof)
Produce enzymes and OSTEOID
- osteocalcin/osteonectin - Ca2+ binding proteins
- collagen Type I
- adhesive proteins - sialoproteins, osteopontin
- proteoglycans
- growth factors and cytokines
- alkaline phosphatase
- osteocalcin/alkaline phophatase markers of blastic activity

express RANKL when stimulated by VitD & PTH
become osteoclasts (trapped in bone)

Increase Activity:

  • PTH
  • embedded cytokines (bone)

Decrease Activity:
- glucocorticoids (apoptosis)

147
Q

Osteoclasts

A

Large multinucleate cells
Derived from haematopoietic stem cells
Secrete acid HCl and protease to destroy/remodel bone
Tartrate-resistant acid phosphatase is marker of osteoclast activity
Stimulated by RANKL and M-CSF from osteoblasts (increased PTH)

Increase Activity:

  • PTH
  • glucocoriticoids

Decrease Activity:

  • Oestrogen
  • Calcitonin
148
Q

Osteocytes

A

Surrounded by bone (osteoblasts left behind)
Maintain bone in response to loading (mechanotransduction)
Osteocyte death -> bone resorption
Sustained by their canaliculae

149
Q

ECF Ca2+ Homeostasis

A

Ca2+ Absorption from intestine
- Vitamin D3, Prolactin

Bone Resorption
- PTH, Vitamin D3, Cortisol

Bone Deposition
- Calcitonin

Kidney Resorption
- PTH (proximal tubule), Vitamin D3 (distal tubule)

Kidney Filtration
- Calcitonin

Vit D & PTH - increases ECF Ca2+
Calcitonin - decreases ECF Ca2+

150
Q

Layers of Epiphyseal Growth Plate

A

Resting Zone - hyaline cartilage
Proliferation Zone - dividing chondrocytes
Maturation Zone - mature chondrocytes
Hypertrophic Zone - dying chondrocytes
Ossification - Degenerating cartilage replaced by bone

151
Q

Myostatin

A

Negative regulator of muscle mass
Prevents muscle proliferation and differentiation

Knockout myostatin increases muscle mass in animals

152
Q

Type I & Type II Muscle Fibres

A

Type I fibres (myosin heavy chain I)

  • slow twitch
  • increased ability to oxidise fat
  • more mitochondria
  • increased rate of disposal of glucose / kg of bodyweight
  • stain dark after acidic preincubation
  • 50% of whole muscle

Type II fibres (myosin heavy chain II)

  • fast twitch
  • 30-50% of whole muscle
  • increased recruitment at high intensity
153
Q

Development of Hip Joint

A

6-9 months

  • femoral head appears (cartilaginous, not calcified)
  • ilium, pubis, ischium not fused

10 years

  • ischium and pubis fused (but not ilium)
  • greater trochanter appears (cartilaginous, not calcified)

12 years
- femoral head fused to femur

14 years
- greater trochanter fused to femur

154
Q

MET

A

Metabolic equivalent
resting oxygen consumption is 1 MET

1 MET = resting metabolic rate
250mL per minute
3.5mL per kilo per minute of oxygen consumption

Greater exercise capability = more METs = reduced risk of disease

155
Q

Exercise Benefit

A
  • lower incidence of CHD
  • reduction in all cause mortality
  • more years of life gained
  • protective qualities on ‘unknown’ CVD risk factors (40%)
  • more effective than drug/surgery for many conditions
  • raised AMPK and PPARδ
AMPK = stress activated kinase in response to energy change in muscle
PPARδ = transcription factor that increases oxidative capacity

***daily sitting time is better predictor of mortality than active/inactive leisure time

156
Q

mTOR vs Foxo

A

mTOR - promotes hypertrophy in response to IGF-1 pathway

Foxo - promotes atrophy (due to lack of IGF-1 or glucocorticoids)

157
Q

Rate of ATP generation

A

PCr - fast but low capacity
Glycolosis - fast but low capacity
CHO oxidation - moderate w/ moderate capacity
Fat oxidation - low w/ infinite capacity

158
Q

Mitochondrial adaptions to exercise training

A
  • increased mitochondrial density
  • increased oxidative enzymes
  • reduced CHO use and lactate production
  • increased fat oxidation
  • enhanced endurance performance
  • improved insulin action (skeletal muscle GLUT4 upregulation)
159
Q

Fuels for sprinting

A
  • primarily PCr, glycolosis, and free ATP

- PCr & ATP fall over duration of sprint

160
Q

Fuels for endurance

A
  • muscle glycogen and glucose usage increase with intensity
  • fat utilisation peaks at aprox 55% intenisty
  • CHO high to begin but decreases over time
  • Fat oxidation increases over time
  • plasma glucose increases over time
161
Q

Muscle response to high intensity resistance training

A
  • neuromuscular changes precede increase in muscle mass

- muscle wasting occurs quickly in response to deloading (esp. myofibril synth rate)

162
Q

Factors influencing exercise metabolism

A
  • exercise intensity and duration
  • diet (high fat = fat oxidation, although limits intensity)
  • training/conditioning (use less CHO and more fat @ same energy expenditure)
  • environmental (high temp = more carb)
  • age & gender (older = more carb due to lower VO2max and working at higher intensity)
  • substrate availability
  • hormone levels
  • skeletal muscle biochemical characteristics
163
Q

Fatigue

A
  • inability to maintain required or expected force or power output
  • due to metabolic feedback from skeletal muscle and lactate
  • can occur at any point along the neuromuscular pathway (e.g. sarcoplasmic reticulum)
  • IMP is indicator of fatigue (breakdown product of excess ADP)
  • greater muscle glycogen (CHO diet) = longer time to fatigue
164
Q

Cardiovascular response to exercise

A
  • Increased O2 supply to skeletal and cardiac muscle
  • microvascular adaptions (increased capillaries)
  • Facilitate CO2 and heat removal
  • Maintain MAP
  • VO2 correlates directly to exercise intensity

VO2 = Q x (CaO2 - CvO2)
oxygen consumption = cardiac output x (oxygen extraction)

Athletes reach same oxygen extraction but higher cardiac output

Athletes have higher SV but lower HR

HR limits diastolic filling and causes plateau of SV

165
Q

Distribution of cardiac flow in response to exercise

A

Muscle > Brain (maintained) > Skin > Gut
skin can constrict to maintain MAP at max intensity
gut can bechome ischaemic

166
Q

Exercise hyperaemia

A

Metabolic vasodilators from muscle, endothelium, RBC

  • endothelium (sheer stress causes release of NO)
  • RBC (unloading of O2)

Muscle pump (venous return)

‘conducted vasodilation’
- spread of vascular smooth muscle depolarisation through gap junctions

functional sympatholysis
- SNS less effective on contracted muscle (so less vasoconstriction)

167
Q

Blood Pressure response to exercise

A

Aortic Systolic (CO) increase
Diastolic (TPR) slight decrease
Overall MAP increase

Baroreceptor reflex reset to allow HR and MAP to increase

HR increases over time
Blood volume decreases (sweating)
SV decreases (fluid loss and increase HR - reduced filling)
TPR increases (to offset SV)

168
Q

Increased Cardiac Output following training

A
  • Expanded Blood Volume (increases EDV and therefore SV)
  • Increased heart size (increased LV mass and chamber size)
  • Increased adrenergic sensitivity (SA node changes)
169
Q

Respiratory response to exercise

A
  • Maintain arterial O2 saturation
  • CO2 removal
  • Acid base balance (lactate)
  • Fluid and temperature balance (animals)
170
Q

Exercise Hyperpnea stimulants

A
  • Motor cortical activation
  • Muscle afferents (spindles, type III & IV)
  • CO2 flux to the lungs (chemoreceptor?)
  • Increased K+, H+, lactate
  • Elevated catecholamines and temp
  • NOT O2!
171
Q

Exercise ventilation following training

A
  • Reduced blood lactate/H+
  • lower plasma K+
  • lower plasma catecholamines
  • reduced activation of muscle afferents?
  • reduced central drive?
172
Q

Heat loss and dehydration during exercise

A
  • at cool temps - primarily convection+conduction
  • at hot temps - primarily sweat+evaporation
  • at hot temps - increased CO to skin w/ decrease SV
  • hot temp correlates with shorter exercise time and lower power output
  • precooling allows for longer performance time
  • intracellular space loses most fluid, then interstitial
  • dehydration reduces exercise time
173
Q

Benefits of fluid ingestion for exercise

A
  • Increased blood volume (therefore SV & CO)
  • Decreased HR
  • lower core temp
  • lower plasma [Na+] and osmolarity
  • reduced muscle glycogen use
  • enhanced exercise performance

Higher sodium ingestion post-exercise increases water balance

174
Q

Exercise for diagnosis

A
  • can use step increments to get an idea of VO2 curves and extrapolate to VO2max
  • high lactate responses at low VO2 correlate to Heart Disease
  • can test PWC150 (i.e. what power output is obtained at HR of 150BPM)
175
Q

Muscle oxidative capacity and endurance

A

Iron is an important component of the ETC -> greater oxidative capacity
increased muscle oxidative capacity is a better predictor of endurance than VO2max

Stronger correlation between lactate and oxidative capacity of muscle than VO2 and oxidative capacity

Higher VO2max at Lactate Threshold correlates to longer time to fatigue
Higher VO2max at Lactate Threshold correlates to lower glycogen used

176
Q

Exercise Benefit vs Risks

A

BENEFITS:

  • typical dose response curve
  • small increase has greatest effect on mortality
  • improved glycemic control in T2DM
  • combined aerobic and resistance best
  • reduction in diabetes risk
  • greater exercise volume = greater VO2max change
  • some may have adverse metabolic responses
  • physical inactivity responsible for more global deaths than smoking
  • increased insulin sensitivity (GLUT4 upregulation)
  • improved fatty acid oxidation (rather than deposition especially in liver)
  • higher levels of HDL
  • reduced visceral obesity
  • reduced blood pressure
  • anti-inflammatory (IL-6)

RISKS:
- Increased risk of sudden death (but lower risk of non-sudden death)

177
Q

Recommended Exercise Reigeme

A

5x30min moderate intensity per week
3x20min high intensity per week
2x strength training (3 sets 8-10reps) per week

178
Q

Stand up intervention

A
  • increase number of breaks in sitting time and reduce overall sitting time
  • pre-assessement with accelerometer
  • intervention session (barriers, benefits, goals etc)
  • sedentary behaviour reduced by 30mins per day
179
Q

In males FSH acts on

A
  • sertoli cells
  • leads to spermatogenesis and cell products
  • androgen binding protein
  • inhibin
  • inhibin negative feedback to anterior pituitary only
180
Q

In males LH influences

A
  • testosterone production (acts on leydig cells)

- testosterone negtive feedback to anterior pituitary and hypothalamus

181
Q

In females FSH causes

A
  • simulation of follicular development (maturation to secondary and tertiary follicle)
  • granulosa cells to produce estrogen & inhibin
  • estrogen has positive feedback on granulosa to produce more estrogen
  • estrogen has negative feedback on anterior pituitary and hypothalamus
  • inhibin has negative feedback on anterior pituitary (decrease FSH - inhibit new follicle)
  • high estrogen stimulates GnRH
  • increasing progesterone stimulates GnRH & LH suge
182
Q

In females LH causes

A
  • stimulation of thecal cells to produce androgens
  • androgens converted to estrogens by aromatase in granulosa cells
  • estrogens negatively feedback on anterior pituitary and hypothalamus
  • inhibin has negative feedback on anterior pituitary (decrease FSH - inhibit new follicle)
  • high estrogen stimulates GnRH
  • increasing progesterone stimulates GnRH & LH suge
183
Q

Human gametes contain how many chromosomes?

A

23

184
Q

Duration of Pregnancy

A 
38 weeks (266 days) from fertilisation
40 weeks (280 days) from last period
185
Q

Periods of Pregnancy

A
  • Early pregnancy (weeks 1 -2)
  • formation of morula and blastocyst implantation
  • not susceptible to teratogens
  • susceptible to chromosomal abnormalities
  • environmental disturbances interfere with implantation
  • Embryonic period (weeks 3-8)
  • most susceptible to teratogens
  • all major organs present at end of week 8
  • Foetal period (weeks 9-term)
  • rapid growth
  • physiological defects (i.e. not enough beta cells)
  • minior morphological abnormalities
  • functional disturbances
186
Q

Hormones produced by the placenta

A 
human chorionic gonadotropin (hCG)
- 'rescue' of corpus luteum (sustains production of hormones)
- high on pregnancy tests
human placental lactogen (hPL)
- breast development
- metabolic effects
estrogen and progesterone
- pregnancy maintenance
- breast development
additional hormones for adaptation to pregnancy
187
Q

Lactation

A

before birth
- prolactin-inhibiting hormone (PIH) blocks prolactin
- high estrogen and progesterone levels suppress milk production
after birth
- high prolactin & low estrogen cause lactation
suckling
- inhibits PIH, allows prolactin to stimulate milk production
- oxytocin stimulates ‘let-down reflex’ - milk ejection (myoepithelial contraction squeezing TDLUs)
- inhibit GnRH and ovarian cycle

188
Q

Determinants of foetal growth

A
  • genetic factors (genotype and sex)
  • IGF, thyroid, insulin promote fetal growth
  • (excess) glucocoritcoids inhibit fetal growth
  • hypoxia
  • hyperthermia
  • toxins (alcohol, drugs, etc)
  • maternal disease / pre-eclampsia
  • malnutrition
  • placental insufficiency
  • oligohydramnios
189
Q

Spermatogenesis

A 
Spermatogonium - (daughter cell on outer edge of seminiferous tubule)
Spermatogonia
Primary Spermatocyte
(first meiotic division)
Secondary spermatocyte
(secondary meiotic division)
Spermatids
190
Q

Oogenesis

A 
Oogonium
(mitotic proliferation)
Primary Oocytes
(arrested in meiosis 1)
Graafian follicle (releases oestrogen) enlargement & Release of oocyte
(completion of meiosis)
Secondary Oocyte & first polat body
(fertilisation &second meitotic division)
Mature Ovum
191
Q

Menstrual Cycle

A

28 days
Two Phases
FOLLICULAR / PROLIFERATIVE PHASE (Oestrogen)
- new layer of endometrium in preparation of pregnancy (becomes a secretory structure)
- follicle growth in ovary (egg matures)
- granulosa cells produce Oestrogen w/ feedback
- days 0-13
OVULATION
- ripened follicles and release of oocytes
- clear non viscous mucous in cervix
- day 14
LUTEAL / SECRETORY PHASE (Progesterone and Oestrogen)
- corpus luteum produces high progesterone and moderate oestrogen
- no new follicle development
- cervical mucous becomes thick and sticky
- conversion of endometrium to secretory structure to promote implantation
- basal body temperature goes up
- ruptured follicle transforms into corpus lutem
- days 15-28
MENSES
- if no pregnancy - bleeding from uterus as endometrium is shed

192
Q

Physiology of Erection

A 
Parasympathetic
 - relaxes cavernosal smooth muscle 
 - dilates arteries (acetylcholine & NO)
 - swelling constricts venous outflow
Sympathetic (loss of erection)
 - restricts inflow
 - constricts cavernosal smooth muscle
193
Q

Effects of HRT (oestrogen)

A

BENEFIT:
- imrpve bone density (decrease resorption)
- relief from flushes, fatigue, and vaginal dryness
- reverse atrophy of vulva, vagina, urethra
- imrprove sleep
- reduced incidence of colorectal cancers
- cardiovascular (reduced CHD?)
- reduced incidence of alzheimer’s?
RISKS:
- fluid retention
- breast tenderness, nausea
- increased risk of breast / uterine cancer
- increased risk of thromboembolism / stroke

194
Q

Oestrogen

A

crosses plasma membrane
acts on cytoplasmic receptors (forms dimer)
dimer binds to oestrogen response element (ERE) for gene expression
monomer + cofactor can lead to gene activation/repression
possible cell membrane receptors with rapid effects
EFFECTS;
- cell growth
- upregulation of progesterone receptor
negative feedback on anterior pituitary
(progesterone feedbacks on hypothalamus also)

195
Q

Testosterone

A 
crosses plasma membrane
acts on cytoplasmic receptors (forms dimer)
dimer binds to response element for gene expression
monomer + cofactor can lead to gene activation/repression
possible cell membrane receptors with rapid effects
EFFECTS;
- gonadotrophin release
- spermatogenesis
- sexual differentiation
- anabolic effects (skeletal growth)
DHT
- prostate development
- external virilisation
- sexual maturation
RISKS:
- increased LDL & decreased HDL
- acne, facial hair, baldness
- menstrual irregularity
- impotence
- gynecomastia
- closure of epiphyseal plates
196
Q

Cell cycle

A 
G0 - resting phase
G1 - cell growth
 - awaiting stimulation to proliferate
 - Ras -> Myc -> -> cyclinD -> initiation of replication
S - DNA replication
G2 - cell increases in size
M - mitosis & cytokinesis
197
Q

Prostaglandin E2

A
  • GPCR agonist at EP(1-4) receptors
  • increase [cAMP] and PKA
  • sensitizes pain mechanisms
  • causes fever
  • vasodilator
198
Q

of
RBCs
WBCs
Platelets

A

RBCs
3-5 x 10^12 / litre
replaced every 120 days

WBCs
2-6 x 10^9 / litre
replaced every 3-5 days

Platelets
150-400 x10^9 / litre
replace every 10 days

199
Q

Tissue Oxygen Delivery Equation

A

= CO x Hb x %Satn x 1.34

200
Q

PCV
MCV
MCH
MCHC

A

PCV = Haematocrit - amount of RBCs

MCV - size of RBCs

MCH - haemoglobin per RBC

MCHC = haemoblobin per unit of RBC

201
Q

What effects result in increased CO?

A
  • Increased blood volume
  • Increased venoconstriction
  • decreased TPR
  • increased contractility
202
Q

ACT
APTT
PT/INR

A

ACT - activated clotting time

APTT - activated partial thromboplastin time
- used to monitor heparin

PT - prothrombin time

INR - (patientPT/normalPT))^ISI
- used to monitor warfarin

203
Q

SA Node pacemaker

A 
Phase 4
Spontaneous depolarisation (Na+in, Ca2+in)

Phase 0
Depolarisation (Ca2+ in)

Phase 3
Repolarisation (K+ out)

ACh/M2(GPCR) - decrease cAMP = opening of K+ channels = slowing of Ca2+ and Na+ influx = slowed phase 4

NA/β(GPCR) - increase cAMP = opening of Ca2+ channels = faster phase 4

204
Q

Ventricular Action Potential

A

Phase 4
stable potential

Phase 0
Depolarisation (Na+ in)

Phase 1
Rapid repolarisation (K+ out)

Phase 2
Plateau (Ca2+ in, K+ out)

Phase 3
Repolarisation (K+ out)

205
Q

Angiotensin II effects

A 
Production of aldosterone (Na, H20 retention)
Vasoconstriction
Cell Growth (cardiac hypertrophy)
Sympathetic stimulation (& increased Renin)

MD1 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions