Week 5 Flashcards

1
Q

What is the meaning of Hepatotropic?

A

Ability to infect hepatocytes (liver cells)

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2
Q

What are the 2 main facts for comparing Hepatitis Viruses A-E?

A
  1. All are hepatotropic

2. All belong to different virus families so possess entirely different properties

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3
Q

What are the viral features of Hepatitis A (HAV)?

A
  • Single-stranded RNA
  • Non-enveloped (naked)
  • Only 1 serotype
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4
Q

What is the transmission of Hepatitis A virus (HAV)?

A
  • Feacal-oral
  • Poor hand hygiene
  • Contaminated food/water (raw shellfish)
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5
Q

What are the 6 stages of infection for Hepatitis A virus (HAV)?

A
  1. Incubation 2-4 weeks
  2. Virus excreted in faeces 1-2 weeks before symptoms
  3. GI tract –> Blood
  4. Infect liver cells
  5. Biliary tract & back to GI tract
  6. Excretion in faeces
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6
Q

What are the clinical features of Hepatitis A virus (HAV)?

A
  • Fever, anorexia
  • Nausea, vomiting
  • Jaundice
  • Dark urine, pale stools
  • Liver enlarged
  • Spleen palpable in 10%
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7
Q

How do you diagnose Hepatitis A virus (HAV)?

A

Presence of anti-HAV IgM

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8
Q

What is the prognosis of Hepatitis A virus (HAV)?

A

Excellent in young adults (0.1% mortality)

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9
Q

What is the treatment for Hepatitis A virus (HAV)?

A
  • No specific treatment
  • Comfort & nutritional balance
  • Fluid & electrolyte replacement
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10
Q

What is the preventative measurements for Hepatitis A virus (HAV)?

A
  • Vaccine
  • Good hygiene
  • Resistant to chlorination
  • Killed by boiling for 10mins
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11
Q

What are the viral features of Hepatitis B virus (HBV)?

A
  • Double-stranded DNA

- Enveloped

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12
Q

What are the 3 different Hepatitis B virus (HBV) antigens?

A
  1. HBsAg- surface antigen
  2. HBcAg- core antigen
  3. HBeAg- envelope antigen
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13
Q

What is the transmission of Hepatitis B virus (HBV)?

A
  • Sexual intercourse
  • Intra-uterine, peri- & post-natal infection
  • Blood
  • Contaminated needles
  • Contaminated haemodialysis equipment
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14
Q

What are the stages of infection for Hepatitis B virus (HBV)?

A
  • Incubation 2-4 months

- 50% develop chronic active hepatitis, 20% of these proceed to cirrhosis, 1-4% risk of these developing liver cancer

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15
Q

What is the definition of Icteric?

A

Jaundice

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16
Q

How do you discriminate between acute & chronic Hepatitis B virus (HBV) infection?

A
  • Both have HBsAg & HBeAg appear during incubation
  • In Acute Antibodies to HBeAg & HBsAg appear
  • In Chronic there is continued presence of HBsAg & absence of antibodies
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17
Q

What are the clinical features of the Pre-icteric period in Hepatitis B virus (HBV)?

A
  • Malaise
  • Anorexia
  • Nausea
  • Pain in right upper quadrant (tender liver)
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18
Q

What are the 3 possible clinical outcomes of Acute HBV infection?

A
  1. Fulminant (sudden) hepatitis
  2. Chronic hepatitis or asymptomatic carrier state
  3. Resolution
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19
Q

What is the treatment for Hepatitis B Virus (HBV)?

A
  • Pegylated interferon (α-interferon)

- Nucleoside analogues such as oral lamivudine

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20
Q

What are the preventative measurements for Hepatitis B virus (HBV)?

A
  • Vaccination (3 injections over 6months)
  • HBV immunoglobulin
  • Blood screening
  • Needle exchange programmes
  • Sexual health education
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21
Q

What are the viral features of Hepatitis C Virus (HCV)?

A
  • 6 virus types
  • Single-stranded RNA
  • Enveloped
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22
Q

What are the clinical features of Hepatitis C virus (HCV)?

A
  • Usually asymptomatic
  • Fatigue
  • Nausea
  • Weight loss
  • Rarely progress to cirrhosis
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23
Q

What may a small proportion of HCV patients develop?

A

Hepatocellular carcinoma

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24
Q

What is the transmission of Hepatitis C virus (HCV)?

A
  • Blood
  • Blood contaminated needles
  • Haemodialysis
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25
Q

What are the stages of infection for Hepatitis C virus (HCV)?

A
  • Replicates mainly in hepatocytes

- Incubation 2weeks - 6months

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26
Q

What type of screening is available for HCV?

A

Blood tests based on NAAT

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27
Q

What are the different treatments for Hepatitis C virus?

combination therapy

A
  • Ribavirin + pegylated α-interferon

- Sofosbuvir (nucleotide analogue)

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28
Q

Is there a vaccine for Hepatitis C virus (HCV)?

A

NO

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29
Q

What are the viral features for Hepatitis D virus (HDV)?

A
  • Small circular single-stranded RNA
  • Defective
  • HDV picks up HBsAg as it buds from liver cell
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30
Q

What is the relationship between HDV & HBV?

A

HBV serves as helper virus for infectious HDV production (co-infection)

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31
Q

What is the transmission of Hepatitis D virus (HDV)?

A

Percutaneously, sexually from infected blood

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32
Q

What are the viral features of Hepatitis E virus (HEV)?

A
  • Single-stranded RNA

- Non-enveloped

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33
Q

What is the transmission of Hepatitis E virus (HEV)?

A

Waterborne disease

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34
Q

What is the stages of infection for Hepatitis E virus (HEV)?

A
  • Peak incidence in young adults
  • Incubation 3-8weeks
  • Self-limiting
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35
Q

When is Hepatitis E virus particularly life threatening?

A

Pregnant women

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36
Q

What are the preventative measurements for Hepatitis E virus (HEV)?

A
  • Good sanitation & hygiene

- Vaccine (Hecolin)

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37
Q

What are 6 other causes of Viral Hepatitis?

A
  1. Epstein-Barr virus
  2. Cytomegalovirus
  3. Yellow fever virus
  4. Adenovirus
  5. Bunyaviruses
  6. Flaviviruses
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38
Q

What is the cloaca separated by?

A

Urorectal septum

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39
Q

What does the urorectal septum separate the cloaca into?

A
  • Anterior: urogenital sinus that is continuous with allantois & form the urethra & bladder
  • Posteror: rectum & upper anal canal
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40
Q

What does lateral folding of the embryo cause?

A

Close body wall & enclose intra-embryonic coelom (peritoneal cavity)

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41
Q

What does the mesoderm form?

A

Somites adjacent to notochord & developing neural tube

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42
Q

What happens to the lateral plate mesoderm?

A

Cavitates to form coelom

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43
Q

What does lateral folding do to the intermediate mesoderm?

A

Becomes posterior abdominal wall

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44
Q

What does the coelom become?

A

Peritoneal cavity

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45
Q

What 4 things are the urinary & reproductive systems derived from?

A
  1. Mesoderm
  2. Coelomic epithelium of posterior abdominal wall
  3. Endodermally derived cloaca
  4. Allantois
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46
Q

Where does the Renal Primordia form?

A

Within the mesoderm of posterior abdominal & pelvic walls

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47
Q

What are the 3 types of sequentially developing Renal Primordia?

A
  1. Pronephros
  2. Mesonephros
  3. Metanephros
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48
Q

What does the mesonephric ducts open into?

A

Cloaca

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49
Q

What happens by the 5th week in Urogenital formation?

A

Ureteric bud extends from mesonephric (Wolffian) duct & induces metanephros that is forming in pelvis & will become the definitive kidney

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50
Q

What does the ureteric bud give rise to?

A
  • Ureter

- Collecting ducts

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51
Q

What does the metanephros become?

A

Renal tissue ie. glomeruli & loops of Henle

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52
Q

When is the kidney functional?

A

10 weeks

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53
Q

What happens if the collecting ducts do not meet the nephric vessels?

A

Cysts form within the kidney

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54
Q

What are the 2 possible abnormalities in Kidney formation?

A
  1. Pelvic kidney

2. Horseshoe kidney

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55
Q

What happens when the ureteric bud branches abnormally before it reaches the metanephric blastema?

A

Abnormal bifid ureter

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56
Q

What happens if the ureteric bud fails to branch at all within the metanephros?

A

Renal agenesis (failure of growth)

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57
Q

What does the urogenital sinus form?

A

Bladder & urethra

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58
Q

What happens to the mesonephric duct once incorporated within urogenital walls?

A

Move caudally to open into the urethra as vas deferent & ejaculatory ducts

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59
Q

What 3 things happen simultaneously in weeks 4 to 6?

A
  1. Cloacal membrane “sinks” into pit of ectoderm
  2. Urorectal septum separates cloaca & becomes perineal body
  3. Cloacal membrane ruptures leaving anal canal & UG sinus is urethral plate
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60
Q

What does the proximal part of the urogenital sinus become?

A

Bladder

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61
Q

What does the allantois form?

A

Closes to become urachus, which may remain patent

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62
Q

What does the pelvic part of the urogenital sinus become?

A

Prostatic & membranous urethrae

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63
Q

How does the paramesonephric duct develop during week 6?

A

Develops lateral to mesonephric duct as an invagination from a cord of coelomic epithelial cells

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64
Q

What does the mesonephric & paramesonephric ducts form?

A

Reproductive ducts & structures

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65
Q

Where are the gonads formed?

A

Mesoderm of the genital ridge

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66
Q

What do germ cells turn into?

A

Cells that produce ova & sperm

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67
Q

What leads to female development from paramesonephric ducts?

A

Absence of Y chromosome & SRY gene

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68
Q

What happens to the mesonephric ducts in the female?

A

Degenerate due to lack of testosterone

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69
Q

What are the Mesonepohric remnants in the female?

A
  • Gartner’s cysts near vagina

- Epoophoron & paroophoron near ovary

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70
Q

When does sexual differentiation occur in the foetus?

A

Week 8

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71
Q

What happens to the paramesonephric ducts in the male?

A

Degenerate but remain as the appendix testis & prostatic utricle

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72
Q

What is the appendix epididymis a remnant of?

A

Proximal end of the mesonephric duct

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73
Q

What happens when the 2 paramesonephric ducts in the female lift off the posterior abdominal wall?

A

Lift peritoneum as the broad ligament

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74
Q

What abnormalities can happen in the female reproductive system?

A

Uterus & vagina may septate & even double

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75
Q

What happens to the male gubernaculum during development?

A
  • Shrinks to draw testis down posterior abdominal wall & through inguinal canal with a loop of parietal peritoneum
  • Testis should be in scrotum at birth
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76
Q

When should the gubernaculum draw the testis through the inguinal canal

A

8th & 9th months

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77
Q

What is the definition of Cryptorchidism?

A

Failure of complete testicular descent into scrotum

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78
Q

What happens to the female gubernaculum during development?

A

Becomes round ligament

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79
Q

What forms the external genitalia?

A
  • Genital tubercle
  • Urogenital/Urethral folds
  • Labioscrotal folds
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80
Q

Describe the development of the male penis?

A
  • Urogenital/Urethral folds form on either side of urethral plate
  • Fuse and create urethral groove
  • Folds & grooves stop at end of genital tubercle (glans penis)
  • Urethral plate continues distally as cord of cells
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81
Q

What is glans hypospadias?

A

Abnormal canalisation of urethra in the glans

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82
Q

What is penile hypospadias?

A

Failure of urethral folds to form, or to extend along the penis & fuse throughout its full length

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83
Q

What is common in the urogenital systems & rectum/anal canal?

A

Connections & fistulae

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84
Q

What are the 6 renal functions?

A
  1. Regulation of ECF volume & blood pressure
  2. Regulation of osmolality
  3. Maintenance of ion balance
  4. Regulation of pH
  5. Excretion of waste
  6. Production of hormones
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85
Q

Describe the 2 part structure of a nephron?

A
  1. Glomerulus: network of capillaries

2. Bowman’s Capsule: double-walled epithelial cup within which the glomerulus is contained

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86
Q

What are the 5 step main processes that occur in the nephron?

A
  1. Filtration by glomerulus
  2. Obligatory absorption & secretion by proximal tubule
  3. Generation of osmotic gradient by loop of Henle
  4. Regulated absorption & secretion by distal tubule
  5. Regulation of water uptake by collecting ducts
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87
Q

What is the triple barrier that glomerular filtration has to occur across?

A
  1. Endothelial lining of capillaries
  2. Basement membrane of capillaries
  3. Foot processes of epithelial cells (podocytes)
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88
Q

What does the triple barrier allow free passage of?

A

Solutes up to ~60kDa

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89
Q

What movement does the triple barrier oppose?

A

Cells & large proteins

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90
Q

What is filtered more in the glomerulus- negatively/positively charged molecules?

A

Negatively charged molecules filtered less easily than positively charged

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91
Q

What forces plasma through the filtration barrier?

A

Hydrostatic pressure

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92
Q

What is R.B.F?

A

Total amount of blood that transverses renal artery/vein per unit time = 1100ml/min

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93
Q

What is R.P.F?

A

Total amount of plasma that transverses renal artery/vein per unit time

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94
Q

How would you work out the R.P.F if the haematocrit is 45% (in a normal adult)?

A

R.P.F = 55% x 1100 = 600ml/min

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95
Q

What affects the production of filtrate?

A

Balance of pressures (Starling forces)

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96
Q

What 2 things FAVOUR movement into tubule?

A
  1. Hydrostatic pressure of blood (+55mmHg)

2. Oncotic pressure of the tubule (0mmHg)

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97
Q

What 2 things OPPOSE movement into tubule?

A
  1. Hydrostatic pressure of tubule (-15mmHg)

2. Oncotic pressure of blood (-30mmHg)

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98
Q

What is the normal glomerular filtration rate (GFR)?

A

125-130ml/min

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99
Q

What 2 things can affect the GFR?

A
  1. Larger bodies have larger GFR

2. GFR falls with age

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100
Q

What are the 3 auto regulation mechanisms of glomerular filtration?

A
  1. Intrinsic/local control
  2. Myogenic mechanism
  3. Tubuloglomerular feedback (nephrogenic)
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101
Q

What is myogenic autoregulation mediated by?

A

Stretch receptors in the arterioles

102
Q

What does constriction in the afferent arteriole cause?

A
  • Reduces filtration pressure

- Glomerular filtration rate (GFR) falls

103
Q

What does constriction if the efferent arteriole cause?

A
  • Pressure to back up within the capillary

- Glomerular filtration rate (GFR) increases

104
Q

What controls GFR?

A
  • Changes to blood flow/pressure
  • Afferent arteriole dilation increases GFR
  • Efferent arteriole dilation decreases GFR
105
Q

What is the total amount of renal blood flow?

A

1 - 1.2L/min (20-25% of cardiac output)

106
Q

Does Renal blood flow (RBF) or Glomerular filtration rate (GFR) change when blood pressure changes?

A

Both essentially constant over wide range of BP

107
Q

How does Tubuloglomerular feedback work?

A
  • Function of juxtamedullary nephron

- Flow in distal tubule indirectly monitored & high flow information fed back to the arterioles

108
Q

What increases when there is high filtrate flow in the distal tubule?

A

Na+ & Ca2+ concentrations

109
Q

What does the Macula densa cells, adjacent to the distal tubule, do?

A
  • Monitors Na+ & Ca2+ levels.
  • Sends signal to the afferent arteriole causing it to constrict.
  • This lowers flow rate to normal limits
110
Q

What 2 types of extrinsic hormonal factors affecting RBF & GFR?

A
  1. Decreased afferent blood flow- VASOCONSTRICTION

2. Increased afferent blood flow- VASODILATATION

111
Q

What extrinsic hormones affecting RBF & GFR cause vasoconstriction?

A
  • Sympathetic nerves release norepinephrine
  • Circulating epinephrine
  • Angiotensin II
112
Q

What extrinsic hormones affecting RBF & GFR cause vasodilatation?

A
  • Renal prostaglandins

- Atrial natriuretic peptide

113
Q

What countries does Squamous cell cancer commonly occur?

A
  • China
  • Iran
  • Central Asia
  • Siberia
  • Mongolia
  • Afghanistan
  • Iceland
  • Finfland
114
Q

What countries does Adenocarcinoma commonly occur?

A

Western population

115
Q

What can invasive oesophageal candidiasis present with?

A

Odynophagia, particularly in areas high HIV

116
Q

What else can be a cause of odynophagia in developing countries?

A

Tuberculosis

117
Q

What are the 3 most common causes of Chronic liver disease?

A
  1. HBV
  2. HCV
  3. Alcohol
118
Q

What tests should be performed on a patient with history of jaundice?

A
  • LFT

- Hepatitis B & C serology

119
Q

When should patients with cirrhosis be treated in a specialised centre?

A

When its complicated by ascites, encephalopathy, bleeding varices or hepatoma

120
Q

What are small-bowel type diarrhoea characteristics?

A
  • Large volume
  • Frothy
  • Greasy
  • Foul-smelling
  • Undigested material
121
Q

What are the large-bowel type diarrhoea characteristics?

A
  • > 6x per day
  • Blood
  • Mucus and/or pus
  • Tenesmus
122
Q

What are the characteristics of diarrhoea when associated with malabsorption?

A
  • Bulky
  • Frothy
  • Greasy
  • Undigested material
123
Q

What are the adult atypical presentations of coeliacs disease?

A
  • Short statue
  • Anaemia
  • Metabolic bone disease
  • Infertility
124
Q

What can TB & chronic amoebiasis present with?

A

Constipation alternating with diarrhoea

125
Q

What are the 3 different classifications of Helminths?

A
  1. Nematodes
  2. Cestodes
  3. Trematodes
126
Q

What 3 places in the body can you find Trematodes infection?

A
  1. Blood
  2. Liver
  3. Lung
127
Q

What 2 places in the body can you find Nematodes infection?

A
  1. Blood & tissue

2. Intestinal

128
Q

What are the 4 different types of host for Helminths infections?

A
  1. Definitive
  2. Intermediate
  3. Accidental
  4. Paratenic
129
Q

Give examples of 4 different vectors & the infections they carry?

A
  1. Flies: Onchoceriasis
  2. Aedes mosquito: Filariasis
  3. Crysops: Guinea worm
  4. Snails: Schistosomiasis
130
Q

What are the 3 different types of transmission for Helminths infection?

A
  1. Faecal oral (Ascaris)
  2. Via vector (Filariasis)
  3. Direct invasion (Schistosomiasis)
131
Q

Give examples of 6 Helminths infections where inflammation is the main pathogenic mechanism?

A
  1. Filariasis
  2. Onchocerciasis
  3. Toxocariasis
  4. Cysticercosis
  5. Schistosomiasis
  6. Enterobius
132
Q

What can repeated cycles of inflammation & bacterial infection caused by Filarial lead to?

A

Acute Lymohoedema –> Elephantiasis

133
Q

What are the clinical features of Trichiuris?

A
  • Vague abdominal symptoms
  • Trichiuris dysentery syndrome
  • Growth retardation
  • Intellectual compromise
134
Q

What are the clinical features of Hookworm?

A
  • Anaemia (adult hookworm takes upto 0.4ml blood)

- Vague abdominal pain

135
Q

What are the clinical features of Ascaris?

A
  • Vague abdominal pain
  • Intestinal obstruction
  • Hepatobiliary obstruction & jaundice
136
Q

What can Cysticercosis cause?

A

CSF obstruction

137
Q

What can cerebral Cysticercosis cause?

A

Seizures

138
Q

What can 3 things can fibrosis of tissue due to Schistosomes cause?

A
  • Right heart failure
  • Portal hypertension
  • Bladder cancer
139
Q

What type of treatment is appropriate for helminth infections causing inflammation?

A

Anti-inflammatory ie. steroids

140
Q

What type of treatment is appropriate for helminth infections causing competition for nutrients?

A

Reduce worm burden & support nutrition

141
Q

What type of treatment is appropriate for helminth infections causing space occupying lesions?

A

Surgery, decompression

142
Q

What type of treatment is appropriate for helminth infections causing stimulation of fibrosis?

A

Helminth eradication & treatment of secondary effects

143
Q

What is the drug treatment for Cestodes?

A

Praziquantel

144
Q

What should you remember when treating Cysticerosis?

A

Necessary to continue anti-epileptic drugs & combine anti-helminthic treatment with steroids

145
Q

What is the main drug treatment for Nematodes?

A

Albendazole

146
Q

What should you remember when treating Nematodes?

A

Single dose/course of treatment is rarely enough as you must engage with the family & environment

147
Q

What are the mechanisms of action of Praziquantel?

A
  • Not fully known
  • Increases calcium permeability of membranes = depolarisation
  • May interfere with purine synthesis
148
Q

What 3 specific infections can Praziquantel be used to treat?

A
  • Hydatid disease
  • Cysticercosis
  • Schistosomiasis
149
Q

What are the possible side effects of Praziquantel?

A
  • Dizziness, headache, drowsiness
  • Abdominal cramps & nausea
  • Diarrhoea
  • Transient asymptomatic rise in transaminases
  • Urticaria, rash and pruritis
150
Q

What can Praziquantel interact with?

A
  • Rifampicin
  • Carbamazine
  • Phenytoin
151
Q

What specific infections can Albendazole be used to treat?

A
  • Nematode infections: trichiuriasis, filariasis
  • Protozoa: giardia
  • Cestode infections: Neurocysticerosis & hydatid disease
  • Other: mebendazole, thiabendazole
152
Q

What are the mechanisms of action of Albendazole?

A
  • Binds to tubules
  • This prevents polymerisation into microtubules
  • Impaired glucose uptake & depleted glycogen stores
  • Degenerative changes appear in worm
153
Q

What are the possible side effects of Albendazole?

A
  • Concentrated in the semen & may be teratogenic
  • Persistent sore throat
  • Headaches, dizziness & seizures
  • Acute liver failure
  • Aplastic anaemia & marrow supression
154
Q

What is the mechanism of action of Piperazine?

A

Agonist activity against the gamma butyric acid receptor paralysing muscular activity

155
Q

What 2 infections is Piperazine used to treat?

A
  • Ascariasis

- Enterobius infection

156
Q

What are the possible side effects of Piperazine?

A
  • GI tract upset

- Rarely hypersensitivity, dizziness

157
Q

What 2 infections is Pyrantel used to treat?

A
  • Hookworms

- Roundworms

158
Q

What is the mechanism of action of Pyrantel?

A
  • Depolarising neuromuscular blockade
  • Excreted unchanged in the faeces
  • Antagonistic with piperazine
159
Q

What is the mechanism of action of Levamisole?

A

Nicotinic acetylcholine receptor antagonist

160
Q

What is Levamisole used to treat?

A

Ascariasis & mixed ascaris hookworm infection

161
Q

What is diethyl carbamazine?

A

Piperazine derivative

162
Q

What is Ivermectin used to treat?

A
  • Fliarial worms
  • Lice
  • Scabies
  • Bed bugs
  • Onchocerciasis
163
Q

What is Niclosamide ONLY used to treat?

A

Tapeworm infections

164
Q

What are the functions of the Proximal Tubule?

A
  • Recovery of ions, sugars, amino acids, peptides & considerable amount of total water
  • Secretes a number of compounds for excretion with urine
  • Metabolises some amino acids
165
Q

What are the 2 pathways molecules & ions can take across the tubule epithelium?

A
  1. Transcellular route (cell body)

2. Paracellular route (leaky ‘tight” junctions between cell bodies)

166
Q

What are the 5 summary points to forces involved in reabsorption from proximal tubule?

A
  1. Ion gradients across the basolateral membrane
  2. Sets up an electrochemical gradient of about -3mV (paracellular efflux of cations)
  3. Osmotic gradient set up by pumping Na out of the cell into the interstitial space
  4. Water moving along the paracellular path due to osmotic pressure drags solutes along with it (solvent drag)
  5. Chemical concentration of solutes left behind facilitates a chemical gradient
167
Q

What is the specific ion gradient across the basolateral membrane?

A

3Na out, 2K in

168
Q

What does the sodium pump (active transport) do in the proximal convoluted tubule cell?

A
  • Na+ concentration gradient

- Gradient used by cell to transport other substances (secondary active transport)

169
Q

What does co-transport with sodium do?

A

Moves substances INTO the cell

170
Q

What does counter transport (exchange) with sodium do?

A

Moves substances OUT of the cell

171
Q

What does the sodium concentration gradient do to H+?

A

Used as an exchanger to transport H+ OUT of the cell (against its concentration gradient)

172
Q

What are the 4 things that happen on the apical membrane of the giant cell?

A
  1. H+ combines with filtered bicarbonate –> carbonic acid which breaks down to H2O & CO2
  2. H2O & CO2 diffuse into the cell
  3. H2O & CO2 produce H+ & bicarbonate
  4. H+ leaves the cell into tubule lumen
173
Q

What 2 things happen in the basolateral membrane?

A
  1. Chloride, bicarbonate & potassium leave down their concentration gradients
  2. Ca2+ is exchanged for Na+. Ca2+ leaves the cell against its concentration gradient
174
Q

What happens to Ca2+ on the apical membrane?

A

Ca2+ enters through a Ca2+ channel

175
Q

How do other solutes enter the renal proximal tubule?

A

Coupled to Na+ entry onto apical membrane, facilitated diffusion on the basolateral membrane

176
Q

What is solvent drag?

A
  • Osmotic gradient from lumen to ISF

- Movement of water (solvent) also “drags” other ions through the paracellular route

177
Q

What is the transport maximum/Tm/Tmax?

A
  • Limit as to how much can be moved

- mg/min or mmol/min (rate)

178
Q

When can Tmac be exceeded?

A

Blood concentration is high (glucose in diabetes mellitus)

179
Q

How is the amount filtered calculated?

A

Amount filtered (mg/min) = Plasma conc. (mg/ml) x GFR (ml/min)

180
Q

What is the reabsorption threshold?

A

Point at which the amount filtered is equivalent to Tmax

181
Q

What happens when you go above threshold?

A
  • Substance appears in urine when normally 100% is reabsorbed
  • Conc of glucose in urine is proportional to plasma conc
182
Q

How much does the Na-glucose transported normally reclaim?

A

~375mg/min glucose

183
Q

What happens if plasma concentration or GFR increases to reabsorption?

A

More than normal limits in the tubule, Tmax may be exceeded as reabsorption process cannot cope

184
Q

What makes up the amount of substance appearing in the urine?

A

Amount filtered + amount secreted

185
Q

What is the movement of Urea in the tubule?

A

Simple diffusion reabsorbs 50-60% (rest lost)

186
Q

What is the movement of lipid-soluble substances in the tubule?

A

Simple diffusion

187
Q

What is the movement of phosphate in the tubule?

A
  • Sodium-linked transport

- Activity of carriers changed by parathyroid hormone

188
Q

What is the movement of protein in the tubule?

A

Small amount digested to amino acids within the tubule cells

189
Q

What the Clearance of a substance excreted by the kidney?

A

Volume of plasma which is cleared of the substance per unit time (ml/min)

190
Q

What is the problem with substance clearance?

A

In reality NO substance is completely cleared during passage through the kidney

191
Q

What are the 3 renal processes which determine & modify the composition of urine?

A
  1. Glomerular filtration
  2. Tubular reabsorption
  3. Tubular secretion
192
Q

What is the range of clearance?

A

From zero (filtered then reabsorbed or never filtered) to equivalent of renal plasma flow (all substance filtered by kidney ends up in urine)

193
Q

What is the Filtration Fraction (F.F.)?

A

GFR (glomerular filtration rate) / RPF (renal plasma flow)

194
Q

What substance has a clearance of zero due to being completely filtered and then reabsorbed?

A

Glucose

195
Q

What substance has a clearance of zero due to never being filtered?

A

Protein

196
Q

How do you work out the renal clearance (Cx)?

A

Cx= Ux x V/Pax

```
V= urine flow rate
(U= urine concentration of x)
(Pa= renal arterial plasma concentration)
~~~

197
Q

What 4 things must a substance be to measure GFR?

A
  1. Freely filtered at glomerulus
  2. Neither secreted or absorbed
  3. Not metabolised
  4. Not toxic
198
Q

What is inulin?

A

Ideal substance but plant sugar & needs to be infused to establish constant plasma concentrations

199
Q

What does a clearance ratio equal, greater and lesser than 1 tell us about the substance?

A
  • Equal to 1 neither secreted of reabsorbed
  • Greater than 1 substance secreted
  • Less than 1 substance reabsorbed
200
Q

What are the 3 stages of Alcoholic Liver disease?

A

Stage 1- Alcoholic fatty liver
Stage 2- Alcoholic hepatitis
Stage 3- Liver cirrhosis

201
Q

Describe Stage 1 Alcoholic fatty liver?

A
  • Build up of fat in liver
  • Can occur quickly
  • Reversible with abstinence
202
Q

Describe Stage 2 Alcoholic Hepatitis?

A
  • Mild can be reversible
  • Major cause of death from liver disease
  • Unrelated to infective hepatitis
203
Q

Describe Stage 3 Liver Cirrhosis?

A
  • Significant scarring of the liver
  • Generally not reversible
  • 50% mortality within 5years if continue to drink
204
Q

What are the different barriers to reducing alcoholic liver disease in Scotland?

A
  • Economic
  • Cultural/behavioural
  • Political
  • Organisational
205
Q

What are the 3 important elements of health promotion?

A
  1. Focus on tackling the determinants of health
  2. Working in partnership with a range of agencies & sectors
  3. Adopting a strategic approach using a range of complementary actions to promote the health of the population
206
Q

Describe the Ottawa Charter for Health Promotion (WHO 1986)?

A
  • Developing personal skills
  • Strengthening community action
  • Reorientation health services
  • Building healthy public policy
  • Creating supportive environments
207
Q

Describe the 3 elements of Tannahill Model of Health promotion?

A
  • Health education
  • Prevention
  • Health protection/Health policy
208
Q

What is the Population approach in health promotion prevention ?

A

Aim is to lower the average level of risk factor in the population

209
Q

What is the High-risk approach in health promotion prevention?

A

People at particularly high risk are identifies through screening, and offered appropriate advice & treatment

210
Q

What is the targeted population approach in health promotion prevention?

A

Identifying communities at greater risk of disease & using population strategies within these targeted groups

211
Q

When is the population approach useful?

A
  • Disease/risk factor is distributed among large proportions of the population
  • Result of not intervening to prevent the disease even in one person are very severe
212
Q

When is the risk approach useful?

A
  • Difficult to change behaviour at population level

- When there is concentrated risk within the population

213
Q

Whose job is it to reduce Alcoholic Liver disease & Alcohol related harm?

A
  • Scottish government
  • Alcohol industry
  • NHS
  • Retailers
  • Police
  • All healthcare workers
  • Teachers
214
Q

What do oxyntic/ parietal cells secrete?

A
  • HCl
  • Pepsinogen
  • Intrinsic factor
  • Mucus
215
Q

What do pyloric glands secrete?

A

Mucus to protect pyloric mucosa and gastrin which stimulates ECL cells

216
Q

What does ECL stand for?

A

Enterochromaffin like cells

217
Q

Where do ECL cells lie?

A

Deep in oxyntic glands

218
Q

What do ECL cells release & in response to what?

A

Histamine in response to gastrin

219
Q

What, other than gastrin, stimulates ECL?

A

Hormones secreted by the enteric nervous system

220
Q

Where is gastrin formed?

A

Antrum of the stomach

221
Q

Which cells secrete gastrin?

A

G cells in pyloric glands

222
Q

What food component has a strong effect on gastrin cells?

A

Proteins

223
Q

What are the 2 polypeptide forms of gastrin?

A
  1. G-34

2. G-17 (more abundant)

224
Q

What 5 things stimulate a reverse enterogastric reflex?

A
  • Food in small intestine
  • Distention of small bowel
  • Acid in upper intestine
  • Presence of breakdown products
  • Irritation of mucosa
225
Q

What does a reverse Enterogastric reflex do?

A

Inhibits gastric secretions

226
Q

Which other hormone inhibits gastric secretion?

A

Secretin

227
Q

How does H. pylori colonise in the stomach?

A

Uses enzyme urease to turn water into ammonia & neutralise gastric acid, allows them to burrow into mucosal surface

228
Q

How does H. pylori damage the stomach?

A
  • Causes mucosal damage by baterial mucinase
  • Inflammation by gastric acids, proteases
  • Leukocyte chemotaxis
  • Mucosal cell death by cytokines & ammonia
229
Q

What 3 things is H. pylori infection directly associated with?

A
  1. Peptic ulcer disease
  2. Gastric carcinoma
  3. MALT lymphoma
230
Q

Describe acute infection of H. pylori?

A
  • Nausea, dyspepsia, malise
  • ~2 weeks
  • Gastric mucosa inflamed with neutrophils & inflammatory cells with marked persistent lymphocyte penetration
  • Stomach acid production falls
231
Q

Describe chronic infection of H. pylori?

A

Local inflammation & gastritis

232
Q

What 5 things does the outcome of chronic H pylori infection depend on?

A
  1. Pattern of inflammation
  2. Host response
  3. Bacterial virulence
  4. Environmental factors
  5. Patient age
233
Q

Describe antral-predominant gastritis?

A
  • Inflammation inhibits D-cells & stimulates G-cells resulting in hypergastrinemia
  • Gastrin –> acid production causing gastric metaplasia of duodenum
234
Q

Describe Pangastritis?

A
  • Inflammation inhibits D-cells & stimulates G-cells resulting in hypergastrinemia
  • Corpus inflammation prevents gastric acid
  • Gastric atropy
235
Q

What are the consequences of a Helicobacter infection?

A
  • Peptic ulcer disease
  • Distal gastric adenocarcinoma
  • Primary gastric MALT
  • Dyspepsia
  • Atrophic gastritis
  • Iron deficiency anaemia
  • Idiopathic thrombocytopaenic purpura
236
Q

Describe the urease breath test?

A
  • Patient swallows urea with carbon 13 inside
  • Urease is present in the stomach, this is converted to CO2 which is breathed out and detected with C13
  • Excess is assumed to be due to H Pylori
237
Q

What are methods of managing peptic ulcer disease?

A
  • Dietary advice
  • Antacids
  • Bismuth
  • Killing H. pylori
  • Proton pump inhibitors
  • H2 blockers
238
Q

What is the treatment for H pylori?

A
  • Proton pump inhibitor

- Ampicillin + clarithromycin/metronidazole

239
Q

What should you give to treat H. pylori if patient is allergic to penicillin?

A

Clarithomycin & Metronidazole

240
Q

How do histamine blocking drugs work?

A
  • Reduce gastric acid by reducing stimulation of oxyntic cells via histamine pathway
  • Permits ulcer healing
241
Q

What are the 2 main histamine blocking drugs?

A
  • Cimetidine

- Ranitidine

242
Q

What are the adverse effects of Cimetidine?

A
  • Dizziness
  • Cytochrome P450 inhibitor
  • Detoxification of other drugs
  • Affects hormone metabolism leading to galactorrhea
  • Interferes with tricyclines and serotonin reuptake
243
Q

What are the adverse effects of Ranitidine?

A
  • Malaise
  • Dizziness
  • Liver toxicity
  • Increase risk of GI infection
244
Q

How is Cimetidine & Ranitidine excreted out the body?

A

Renal excretion

245
Q

Give 1 example of a Proton pump inhibitor used to treat H. pylori?

A

Omeprazole

246
Q

What are the adverse effects of Omeprazole?

A
  • Headaches
  • Dizziness
  • Upper respiratory tract infection
  • Abdominal pain
  • Back pain
  • Rash
247
Q

What are the alternative antibiotics you can used for treatment of H. pylori?

A

Fluoroquinolones

248
Q

How common is failure of the initial course for peptic ulceration?

A

1 in 5

249
Q

What is the 2nd line of treatment for peptic ulceration?

A
  • Alternative regimen

- Quadruple (PPI + bismuth + 2 antibiotics)

250
Q

What is Galactorrhae

A

Breasts produce & leak milk