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BRS > Hard flashcards > Flashcards

Hard flashcards

1
Q

Ankylosing spondylitis extra articular features?

A

4 A’s. Anterior uveitus. Apical lung fibrosis. Aortitis. Amyloidosis.

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2
Q

Serious infections that can cause reactive arthritis?

A

HIV. Hepatitis C.

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3
Q

Reactive arthritis extra articular features?

A

Skin inflammation. Eye inflammation. Enthesitis.

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4
Q

Psoriatic arthritis presentation?

A

Scaly red plaques on extensors. Assymetrical joint involvment. Interphalangeal joints affects not MCP joints.

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5
Q

What hormones do sertoli cells produce?

A

Anti mullerian hormone, Androgen binding hormone, inhibin and activin.

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6
Q

What is menarche?

A

First menstrual period.

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7
Q

Describe folliculogenesis?

A

Primordial follicle to primary follicle. Primary follicle has layers of theca and granulosa cells. Development of secondary follicle. Secondary follicle has FSH and LH receptors and has fluid filled cavity. Surge in LH causes development of mature follicle. Follicle ruptures, ovum released. Formation of corpus luteum - progesterone and oestradiol release.

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8
Q

What do theca cells do?

A

Androgen synthesis. Structural support to growing follicle.

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9
Q

What stimulates granulosa cells?

A

FSH.

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10
Q

What happens to granulosa cells after ovulation?

A

Formation of corpus luteum. Granulosa cells converted to granulosa lutein cells. Granulosa lutein cells secrete progesterone and relaxin.

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11
Q

What inhibits GnRH, LH and FSH release?

A

Oestrogen, progesterone and testosterone.

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12
Q

Symptoms hyperprolactinemia?

A

Amenorrhoea, osteoporosis and low libido.

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13
Q

How to check if a woman has ovulated?

A

Day 21 progesterone test and ultrasound.

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14
Q

What occurs in the decidualisation phase?

A

Changes in endometrium.

  • Glandular epithelial secretion
  • Production of glycogen in stromal cell cytoplasm.
  • Growth of capillaries
  • Increase in vascular permeability cause oedema.
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15
Q

What factors mediate blastocyst adhesion? What cell releases these?

A

Leukaemia inhibitory factor and IL-11. Endometrial cells.

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16
Q

Elevated maternal hormones during pregnancy?

A

ACTH, Adrenal steroids, T3 and T4, IGF-1, PTH peptides and Prolactin.

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17
Q

Describe the follicular phase?

A

Rise in FSH causes growth of follicles. Secretion of oestradiol and inhibin B from follicles inhibits FSH secretion. Only dominant follicle survives. Oestradiol continues to increase; switch to positive feedback causes a surge in LH which causes ovulation.

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18
Q

What occurs in the proliferative cycle of the endometrium cycle? What hormone drives this?

A

Epithelial growth, increase in arterioles. Oestradiol.

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19
Q

What occurs in the secretory phase of endometrial cycle?

A

Secretion of glycogen. Increase in volume of stromal cells produces thick lining.

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20
Q

What is another name for secondary hypogonadism?

A

Hypogonadotrophic hypogonadism.

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21
Q

Menopause biomarkers?

A

Low AMH, High FSH/LH, low oestrogen and low inhibin.

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22
Q

What cause premature ovarian syndrome?

A

Turners syndrome, autoimmunity and chemo/radiotherapy.

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23
Q

Example of an aromatase inhibitor?

A

Anastrozole.

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24
Q

Describe intramembranous ossification?

A

MSC’s form osteoblasts. Osteoblasts cluster together and secrete osteoid which traps osteoblasts to form osteocytes. MSC’s form periosteum and formation of trabecular matrix occurs. Crowded red blood cells condense to form red bone marrow.

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25
Q

What is concentric lamellae?

A

Rings of bone matrix.

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26
Q

What is lacunae?

A

Between rings contain osteocytes.

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27
Q

What is the function of osteoblasts?

A

Form bone by secreting osteoid and catalysing mineralisation of bone.

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28
Q

What is inorganic bone matrix?

A

Calcium hydroxyapatite and osteocalcium phosphate.

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29
Q

Process of endochondral ossification?

A

Bone collar forms around diaphysis of the hyaline cartilage model. Cartilage calcifies in the center of the diaphysis and then develops cavities. Blood vessel of periosteal bud invades internal cavities and formation of cancellous bone occurs. Diaphysis elongates and medullary cavity forms. Secondary ossification centre develops after birth at epiphysis. Ossification occurs at epiphysis; cartilage replaced by bone. Eventually only cartilage left is at epiphyseal plate and articular cartilage.

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30
Q

What cell types does the periosteal bud contain?

A

HSC’s, osteoblasts and osteoclasts.

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31
Q

What is the epiphysis?

A

Zone between epiphyseal plate and joint.

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32
Q

What breaks down cartilage?

A

Osteoclasts.

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33
Q

What is interstitial bone growth?

A

Increase in bone length.

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34
Q

What is appositional bone growth?

A

Increase in bone thickness.

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35
Q

What occurs at the diaphyseal side in interstitial growth?

A

Cartilage calcifies and dies. Replaced by bone.

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36
Q

Explain how appositional bone growth occurs?

A

Ridges form at periosteum parallel to blood vessel. Ridges fuse and form tunnel around blood vessel. Osteoblasts in the endosteum, build new concentric lamellae inwards towards centre of tunnel forming a new osteon. Bone grows outwards as osteoblasts in periosteum build new circumferential lamellae.

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37
Q

Risk factors for osteoporosis?

A

Age, sex, alcohol intake, glucocorticoid use and hypogonadism.

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38
Q

How does vitamin D deficiency cause osteomalacia/rickets?

A

Lower blood calcium results in less mineralisation of bone.

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39
Q

How does congential osteogenesis imperfecta affects bones?

A

Insufficient osteoid production.

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40
Q

What occurs to bone in pagents disease?

A

Excessive bone break down and disorganised remodelling.

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41
Q

What metastases cause bone growth?

A

Prostate metastases.

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42
Q

What metastases can have blastic and lytic effects on bone?

A

Breast metastases.

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43
Q

What metastases can have a lytic affect on bone?

A

Kidney, thyroid and lung metastases.

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44
Q

Secondary bone healing process overview?

A

Haematoma formation, release of cytokines and angiogenesis at fracture. Formation of soft callus and formation of hard callus. Excess of bone is removed.

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45
Q

Two different of ways of holding bone? What is the difference?

A

Closed (non invasive) and fixation (surgical intervention).

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46
Q

Two examples of closed ways of holding a bone?

A

Cast and traction.

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47
Q

What is a closed fracture? What can it lead to?

A

Broken bone but skin intact. Can result in compartment syndrome.

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48
Q

4 stages of healing of ligament or tendon?

A

Bleeding, inflammation, proliferation and remodelling.

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49
Q

How does the ACL provide stability?

A

Prevents tibia from going too far forward. Limits rotational movement.

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50
Q

Transient synovitis treatment?

A

NSAID’S.

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51
Q

What can a tear to the meniscus cause?

A

Locked knee.

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52
Q

Treatments for osteoporosis?

A

SERMS, Bisphosphonates and HRT.

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53
Q

Cortisol hormone effects apart from raising blood glucose?

A

Increases vascular permeability and urine output.

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54
Q

Explain the electrical activity in the heart?

A

Primary pacemaker signal is generated in the SAN. Electrical signals is transmitted across the myocardium of atrium along the internodal tracts. Slowing down of electrical signal at AV node. Transmission of electrical signals along bundle of his down intravetrincular septum to apex of heart. Transmission of electrical signals along the purkinje fibers cause contraction of ventricles.

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55
Q

When is preload increased in the heart?

A

Hypervolemia, regurgitation of aortic and pulmonary valve (leaky heart valves - don’t close fully), heart failure.

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56
Q

How is afterload measured?

A

End systolic volume.

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57
Q

How does the left ventricle walls experience similar tension to right ventricles?

A

Left ventricles have a low radius of curvature (radius) and a higher pressure.

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58
Q

When would you have a 4th heart sound?

A

During atrial systole. In patients with congestive heart failure, pulmonary embolism or tricuspid incompetence (regurgitation).

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59
Q

When is S1 sound produced?

A

Isovolumetric contraction.

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60
Q

When is QRS complex produced?

A

Isovolumetric contraction.

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61
Q

When is T wave produced?

A

Reduced ejection.

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62
Q

What phase of cardiac cycle is the dichrotic notch present in?

A

Isovolumetric relaxation.

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63
Q

When would you have a 3rd heart sound?

A

During rapid passive filling. Patients with severe hypertension or mitral incompetence.

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64
Q

Explain how noradrenaline or adrenaline can cause changes in cardiac contractility?

A

Noradrenaline or adrenaline bind to beta 1 or beta 2 receptors. This triggers a g protein to activate adenylyl cyclase. Adenylyl cyclase converts ATP to cAMP (cyclic adenosine monophosphate). cAMP activates PKA (protein kinase A). PKA phosphorylates the L-type calcium channel and the ryanodine receptor. This leads to more calcium entry and calcium release. More calcium delivery to myofilaments results in more force produced. PKA also phosphorylates SRCa2+ATPase allowing for more take up of calcium to prepare for next contraction.

65
Q

Explain airway constriction by nerves

A

Solid enters airway and detected by sensory receptors. Excitation of sensory nerves up to brain stem, Excitation of parasympathetic nerves cause release of ACh from preganglionic terminal ends. This results in release of ACh from post ganglionic fibres. ACh cause contraction of smooth muscle in airways and mucus secretion.

66
Q

Intrinsic anabolic and anti-catabolic factors for articular cartilage in joints?

A

Tissue inhibitor of metalloproteinases. Growth factors.

67
Q

What are the molecular changes present during osteoarthritis?

A

Proteoglycan fragmented by aggrecanases. Collagen broken down by collagenases (MMP).

68
Q

What early changes in cartilage would be present in early osteoarthritis?

A

Loss of proteoglycan in superficial zone leads to fibrilation.

69
Q

What late changes in cartilage would be present in late osteoarthritis?

A

Fissuring deep into cartilage matrix, loss of cartilage thickness, formation of osteophytes and bone cysts. Synovial inflammation.

70
Q

Where does hand osteoarthritis occur?

A

Distal interphalangeal joint, proximal interphalangeal joint and trapeziometacarpal joint (base of thumb OA).

71
Q

OA treatment?

A

Total joint replacement. Trapeziectomy

72
Q

Explain the steps leading to the initial muscle contraction

A

Action potential occurs at the presynaptic terminal. Activation of calcium voltage gated channels causes release of calcium which causes exocytosis of vesicles contain acetylcholine. Acetylcholine diffuses across synaptic cleft and bind to acetylcholine receptors on the muscle. This results in an action potential spreading across the surface of the muscle fiber membrane. ACh is broken down by acetylcholine esterase.

73
Q

Explain the steps in the initial muscle contraction after an action potential has arrived

A

Action potential propagates across surface of muscle membrane and T tubules. DHP receptor detects voltage and results in a change in the shape of the protein linked to the ryanodine receptor. This opens the ryanodine receptor and results in calcium leaving the sarcoplasmic reticulum and traveling deep into the muscle fiber where it binds to troponin. This causes tropomyosin to move and expose myosin binding sites. Myosin head forms a cross bridge with actin. Release of ADP and phosphate allows myosin to produce power stroke and pull actin towards centre of sarcomere. ATP binding releases myosin head from actin chain and ATP hydrolysis recharges myosin head. Calcium is actively transported back into SR while action potential continues.

74
Q

Structure of a slow motor unit?

A

Small cell bodies. Small dendritic trees. Thin axons.

75
Q

Structure of a fast motor unit?

A

Large cell bodies. Large dendritic trees. Thick axons.

76
Q

Insulin blood glucose reducing mechanisms

A

Build up of glycogen stores, breakdown of glucose (increased rate of glycolysis), increased uptake of glucose via GLUT4 transporter, increased protein synthesis, increased lipogenesis and decreased lipolysis.
Decreases gluconeogenesis and ketogenesis.

77
Q

Beta cells release of insulin mechanism

A

Glucose binds to GLUT 2 without the need for insulin. Glucose gets converted to glucose -6-phosphate which results in an increase in ATP. Increase in ATP results in closure of potassium channels which increases levels of potassium in the cell. This results in opening of calcium channels allowing movement of calcium into cell. Calcium moving into cell causes release of insulin.

78
Q

What hormones promote protein synthesis in muscle?

A

Insulin, GH and IGF-1.

79
Q

What hormones stimulate amino acid use for gluconeogenesis in liver?

A

Glucagon, cortisol.

80
Q

What hormone stimulates protein breakdown in the liver?

A

Glucagon.

81
Q

What hormones stimulate breakdown of triglycerides in adipocytes so that glycerol and fatty acids can be released into the blood?

A

Cortisol and growth hormone.

82
Q

What hormones stimulate conversion of glycogen to glucose-6-phosphate (glycogenolysis)?

A

Glucagon and adrenaline (during fight and flight).

83
Q

What hormones inhibit uptake of glucose via GLUT4 on muscle cells?

A

Glucagon and growth hormone.

84
Q

Symptoms of type 1 diabetes?

A

Weight loss, hyperglycemia, glycosuria with osmotic symptoms (polyuria, nocturia and polydipsia). Ketones in blood and urine.

85
Q

Diagnostic tests for type 1 diabetes?

A

Antibody tests - GAD and IA2
C - peptide
Presence of ketones

86
Q

When a large fracture where bone edges are not close and there is low stability what occurs at the fracture?

A

Haematoma formation, release of cytokines and angiogenesis at fracture. Soft callus formation which is converted to a hard callus. Excess bone is removed.

87
Q

What maternal hormones are lowered during pregnancy?

A

FSH and LH. GH and TSH.

88
Q

Types of capillary structures?

A

Continuous, fenestrated and discontinuous.

89
Q

What is dead space?

A

Part of lungs where there is no gas exchange.

90
Q

What is dalton’s law?

A

Pressure of gas mixture is equal to sum of partial pressure of gases in the mixture.

91
Q

What does carbon monoxide do to blood O2 and HbO2 saturation?

A

Low blood O2 as its harder to release oxygen from carbon monoxide bound haemoglobin. Reduced HbO2 saturation as haemoglobin binds to carbon monoxide instead of oxygen.

92
Q

Why may the blood leaving the lungs not have 100% HbO2?

A

Due to bronchial circulation drainage of deoxygenated blood into pulmonary vein

93
Q

Why does resistance to airflow decrease later in inspiration?

A

Greater lung volume and more dilated airways results in lower resistance.

94
Q

What is laminar blood flow?

A

Velocity of fluid is constant at any one point and flow in layers. Blood flows fastest closest to the centre of lumen; blood cells closest to the wall experience more friction.

95
Q

What is turbulent blood flow?

A

Blood flows in irregular manner and is prone to pooling.

96
Q

How do you calculate pulse pressure?

A

Systolic blood pressure - diastolic blood pressure.

97
Q

How does an aneurysm happen?

A

Weak muscle fibres in artery wall. Inward force produced by artery wall doesn’t match the blood pressure and so blood vessel expands until it ruptures.

98
Q

When standing upright, why does the bottom of the lung have greater ventilation?

A

Smaller and more compliant alveoli at the bottom of the lungs and effects of gravity.

99
Q

Epithelial structure of oesophagus?

A

Non keratinising stratified squamous epithelium.

100
Q

Describe swallowing

A

Pharyngeal musculature guide bolus towards oesophagus. Both oesophageal sphincters open. Upper sphincter closes. Superior circular muscles contract and inferior rings dilate. Sequential contractions of longitudinal muscle moves food. Lower sphincter closes as food moves through.

101
Q

What is the epithelial transition from oesophagus to stomach?

A

Stratified squamous to simple columnar.

102
Q

What does the cardia and pyloric region of the stomach contain?

A

Mucus only.

103
Q

What does the body and fundus of the stomach contain?

A

Mucus, HCL and pepsinogen.

104
Q

What does the antrum of the stomach contain?

A

Gastrin.

105
Q

What layer of the stomach wall are tubular glands present in the stomach?

A

Mucosa.

106
Q

What nervous system is responsible for segmentation? What activates it?

A

Stretching of muscle activates enteric nervous system.

107
Q

How are parietal cells adapted?

A

Contain lots of mitochondria as they require lots of ATP. Intercanaliculi that increases surface area for secretion.

108
Q

What do the cytoplasmic tubulovesicles in the parietal cells contain? What do they do?

A

H+/K+ATPase. Fuse with canaliculi.

109
Q

What does gastrin act on?

A

Receptors on parietal cell and Enterochromaffin-like cells.

110
Q

How does acid release from parietal cells act on a negative feedback system?

A

Inhbits gastrin release to prevent further acid release.

111
Q

What structures also produce bicarbonate instead of bicarbonate present in pancreatic juice?

A

Bile from liver and alkaline fluid from brunners glands.

112
Q

What does lipase require for action?

A

Colipase and bile salts.

113
Q

During cephalic and gastric phase what is mainly secreted in the pancreatic juices?

A

Enzyme rich juice. Lacks carbonate.

114
Q

What stimulates release of cholecystokinin?

A

CCK releasing peptide due to increase in amino acid and fatty acids in lumen of duodenum. Gastrin releasing peptide.

115
Q

What inhibits release of CCK?

A

Trypsin.

116
Q

What kind of cells are enterocytes?

A

Columnar epithelium.

117
Q

What do paneth cells do?

A

Regulate intestinal flora and engulf some bacteria.

118
Q

What distinguishes the duodenum from the jejunum and ileum?

A

Presence of brunner’s glands.

119
Q

What distinguishes the jejunum from the ileum?

A

Ileum has thin wall while jejunum has thick wall.

120
Q

How are glucose and galactose absorbed?

A

Secondary active transport by SGLT1 (sodium/glucose cotransporter 1) carrier protein on apical membrane.

121
Q

How is fructose absorbed?

A

GLUT5 by facilitated diffusion on apical membrane.

122
Q

What transporter on enterocytes absorb small peptides?

A

PepT1.

123
Q

What are the steps of lipid digestion?

A

Mechanical emulsification of lipids in stomach. Secretion of bile salts and pancreatic lipases. Emulsification of lipids. Lipase activated by co-lipase. Enzymatic hydrolysis of ester linkages. Solubilisation of lipolytic products in bile salt micelles (holds lipolytic products).

124
Q

What does a crescendo decrescendo murmur indicate?

A

Atrial stenosis (valve narrowing).

125
Q

Most common cause of mass in atria?

A

Atrial fibrilation. Blood not pumping properly so formation of blood clot.

126
Q

What are the 3 phases of nodal cell action potential?

A

Prepotential (phase 4), upstroke (phase 0) and repolarisation (phase 3). Continually repeats.

127
Q

In a nodal cell action potential what causes the upstroke phase?

A

Calcium influx.

128
Q

In a nodal cell action potential what causes the repolarisation phase?

A

Potassium efflux.

129
Q

In a nodal cell action potential what causes the prepotential phase?

A

Sodium influx.

130
Q

5 phases of cardiac muscle action potential?

A

Upstroke (Phase 0), Early repolarisation (Phase 1), Plateau (phase 2), repolarisation (phase 3), Resting membrane potential (phase 4).

131
Q

How does sympathetic nervous system act on the kidneys to increase blood volume?

A

Acts on alpha one adrenoreceptor to cause vasoconstriction of afferent arteriole that enters glomerular capsule. Decrease in glomerular filtration which results in decreased sodium excretion. Increase in blood volume.

132
Q

What receptor do sympathetic nerves act on to secrete renin?

A

Beta 1 adrenoreceptor.

133
Q

What nerves do volume and pressure sensors send signals through?

A

Glossopharyngeal and vagus nerves.

134
Q

What does constriction of veins do to venous return?

A

Increases venous return.

135
Q

Where are volume sensors in cardiovascular system?

A

Large pulmonary vessels, right atria.

136
Q

Where are pressure sensors in the cardiovascular system?

A

Aortic arch and afferent arterioles in the kidney.

137
Q

Local vasodilators?

A

Nitric oxide and prostacyclin.

138
Q

Local vasoconstrictors?

A

Thromboxane A2 and endothelins.

139
Q

Systemic vasodilators?

A

Kinins (stimulate NO synthesis) and atrial natriuretic peptide (ANP).

140
Q

When is atrial natriuretic peptide released?

A

Secreted from the atria in response to stretch

141
Q

What does peptide YY do?

A

Reduce intestinal motility, gallbladder contraction and pancreatic exocrine secretion.

142
Q

What cells secretes GIP and where are these cells located?

A

K cells in duodenum and jejunum.

143
Q

What bile salt uptake channels are present in hepatocytes?

A

organic anion transporting peptides (OATPs) and Na+ taurocholate-cotransporting polypeptide (NTCP).

144
Q

What bile salt export channels are present in hepatocytes?

A

Bile salt excretory pump (BSEP)
MDR (multi drug resistant) related proteins
MDR1 and MDR3

145
Q

What do MDR (multi drug resistant) related proteins like MRP2 and MRP3 export into bile?

A

Negatively charged metabolites.

146
Q

What do MDR1 channels export into bile?

A

Excretion of neutral and positive xenobiotics.

147
Q

What do MDR3 channels export into bile?

A

Phospatidylcholine.

148
Q

What happens when bilirubin from the blood arrives in the liver?

A

Conjugated with 2 molecules of UDP-glucuronate to produce bilirubin diglucuronide. Secreted into biliary canaliculi.

149
Q

What happens when monoglycerides and fatty acids enter the enterocytes?

A

Reconstructed back into triglycerides by Monoglyceride acylation, Phosphatidic acid pathway. Incorporated in chylomicrons and secreted across basement membrane by exocytosis into lymph vessel.

150
Q

What occurs when there is excessive inflation of lungs?

A

Pulmonary stretch receptors activated. Inhibition of dorsal respiratory group and apneustic centre and stimulation of ventral respiratory group. Inspiration inhibited and expiration stimulated.

151
Q

What neurones connected to muscles cause increase in breathing rate when muscles move?

A

Proprioceptive afferent neurones from golgi tendon organ (responds to stretch on tendon) and muscle spindle (stretch receptors).

152
Q

How is sodium absorbed in the ileum?

A

Secondary active transport. Co-transport with chloride ions.

153
Q

Where is calcium absorbed?

A

Duodenum and ileum.

154
Q

Explain B12 absorption

A

Haptocorrin binds to B12. Parietal cells in stomach secrete intrinsic factor which binds to B12. B12 intrisic factor complex binds to cubilin receptor and taken up in distal ileum. B12 intrinsic factor complex broken down in enterocyte and b12 binds to transcobalamin II (TCII) where it then crosses basolateral membrane into blood. Taken to liver where TCII is broken down.

155
Q

How does defecation occur?

A

Distension of walls of rectum. Pressure receptors send signals via myenteric plexus to initiate peristaltic waves in descending, sigmoid colon and rectum. Internal anal sphincter inhibited. External anal sphincter under voluntary control.

156
Q

What are the two ways in which GFR is regulated?

A

Myogenic mechanism and tubulo-glomerular feedback mechanism.

157
Q

How does tubulo-glomerular feedback mechanism regulate GFR if GFR rises?

A

Increase in GFR. Increase in sodium chloride in loop of henle. Change detected by macula densa. Increase in ATP release. Adenosine removed from ATP and so increase in adenosine released. This signal results in constriction of arteriole. Blood flow reduces and GFR therefore stays the same.

158
Q

What does extracellular/intracellular activation of trypsin in pancreatitis result in?

A

Activation of elastase which causes vessel destruction and islet necrosis leading to bleeding and hyperglycemia. Activation of complement also causes vessel destruction. Activation of prothrombin leads to thrombosis which leads to ischaemia. Activation of phospholipase A2 leads to fat necrosis which leads to hypocalcemia. Activation of kallikrein leads to vasodilation and plasma exudation that can lead to shock.

159
Q

How does formation of the neural tube happen?

A

Notochord signals direct the neural plate ectoderm to invaginate to form the neural groove. This create two neural folds that run along cranial caudal axis. Neural folds move together over neural groove and fuse forming a hollow tube. Migration of neural crest cells to other tissues.

BRS (52 decks)

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