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Question 1

An example of normocytic anaemia is
A.	Iron deficiency
B.	Vitamin B12 deficiency
C.	Anaemia of chronic disease
D.	Haemolytic anaemia
E.	Folate deficiency

Answer 1

C. Anaemia of chronic disease

Question 2

Choose the one incorrect statement
A. Supra renal glands are superior to kidneys
B. The liver is in direct contact with the right kidney
C. The duodenum is medial to the right kidney
D. The tail of the pancreas is anterior to the left kidney
E. The small intestine is medial to the left kidney

Answer 2

B. The liver is in direct contact with the right kidney

Question 3

When referring to the cortico-medullary gradient what is the osmolarity of the medullary region of the kidneys
A.	300 mosmol/L
B.	900 mosmol/L
C.	1400 mosmol/L
D.	1200 mosmol/L
E.	600 mosmol/L

Answer 3

D. 1200 mosmol/L

Question 4

Which one of the following drugs should not be taken while breastfeeding?
A. Warfarin
B. Loratadine
C. Tramadol
D. Amoxicillin
E. Enoxaparin

Answer 4

C. Tramadol

Question 5

Which ONE of the following is not a possible cause of microcytic (iron deficiency) anaemia
A.	Poor iron intake from the diet
B.	Blood donation
C.	Taking NSAIDs
D.	Intrinsic factor receptor deficiency
E.	Gastro-intestinal disorders

Answer 5

D. Intrinsic factor receptor deficiency

Question 6

Which One of the following is incorrect?
A. The normal bilirubin range is 3-21 micromol/L
B. Normal white blood cell count is 3-10x 109/L
C. The normal urea level is 2.5-6.5 mmol/L
D. The normal potassium level is 35-53mmol/L
E. Normal blood pressure range is 90/60 to 120/80 mmHg

Answer 6

D. The normal potassium level is 35-53mmol/L

should be 3.5-5.3

Question 7

Which One of the following options represents the response of renal arterioles to a decrease in blood pressure to maintain GFR?
A. Afferent arterioles dilate, Efferent arterioles constrict
B. Afferent arterioles constrict, Efferent arterioles constrict
C. Afferent arterioles dilate, Efferent arterioles dilate
D. Afferent arterioles constrict, Efferent arterioles dilate
E. No response

Answer 7

A. Afferent arterioles dilate, Efferent arterioles constrict

Question 8

What is the function of ADH in the kidney?
A. Increases water loss by inhibition of reabsorption via aquaporins
B. Increases loss of water in the filtrate
C. Acts as a pore so that water is reabsorbed into the blood
D. Signals for the placement of aquaporins in the apical and baso-lateral membranes allowing for movement of water from the blood to filtrate
E. Signals for the placement of aquaporins in the apical and baso-lateral membranes allowing for movement of water from the filtrate to blood

Answer 8

E. Signals for the placement of aquaporins in the apical and baso-lateral membranes allowing for movement of water from the filtrate to blood

Question 9

Which is the main cell that is involved in destruction of beta cells in the pancreas in type 1 diabetes?
A.	T cells
B.	B cells
C.	Neutrophils
D.	Macrophages
E.	Eosinophils

Answer 9

A. T cells

Question 10

What is meant by adverse drug reaction?
A. A noxious and unintended response to a drug that occurs at doses used for prophylaxis, diagnosis or therapy but response may not be due to that specific drug
B. An allergy to that specific drug
C. A noxious and unintended response to a drug that occurs at doses used for prophylaxis, diagnosis or therapy
D. Reactions are always dose related and predictable

Answer 10

C. A noxious and unintended response to a drug that occurs at doses used for prophylaxis, diagnosis or therapy

Question 11

What is the most likely function of the proximal convoluted tubule?
A. Passive reabsorption of water only
B. Active transport of sodium
C. Active reabsorption of urea and hydrogen ions
D. Active transport of sodium and glucose
E. Regulate blood pressure, helping to release renin

Answer 11

D. Active transport of sodium and glucose

Question 12

Which of the following has a rate of urinary excretion that is always much lower than its rate of glomerular filtration in a healthy adult?
A.	Urea
B.	Potassium
C.	Sodium
D.	Glucose
E.	Calcium

Answer 12

D. Glucose

Question 13

Which one of the following is an accessory inspiratory muscle?
A.	Internal intercostal
B.	External intercostal
C.	Internal oblique
D.	Rectus abdominus
E.	Diaphragm

Answer 13

B. External intercostal

Question 14

Which of the following options is characteristically involved in the initial response in acute inflammation?
A. Constriction of arterioles
B. Capillary endothelial cell enlargement
C. Influx of macrophages
D. Influx of mast cells
E. Influx of neutrophils

Answer 14

E. Influx of neutrophils

Question 15

How does activated Vitamin D directly maintain normal serum calcium
A. Decreases calcium absorption from the intestinal lumen
B. Increases calcium release from bone
C. Increases calcium reabsorption from the kidney tubule
D. Decreases calcium reabsorption from the kidney tubule
E. Increases calcium release from the stomach

Answer 15

C. Increases calcium reabsorption from the kidney tubule

Question 16

What renal compensation takes place for respiratory alkalosis?
A. Less renal excretion of bicarbonate ions and less renal absorption of hydrogen ions
B. More renal excretion of bicarbonate ions and more renal absorption of hydrogen ions
C. More renal excretion of hydrogen ions and more renal absorption of bicarbonate ions
D. More renal excretion of carbon dioxide
E. Less excretion of carbon dioxide

Answer 16

B. More renal excretion of bicarbonate ions and more renal absorption of hydrogen ions

Question 17

Which one these statements correctly explains the hygiene hypothesis?
A. Decrease in allergic disease is due to reduced exposure to pathogen
B. Increase in allergic disease is due to reduced exposure to pathogen causing a decreased default Th2 differentiation
C. A decreased default Th1 differentiation
D. An increase in allergic disease is due to reduced exposure to pathogen causing a increased default Th2 differentiation

Answer 17

D. An increase in allergic disease is due to reduced exposure to pathogen causing a increased default Th2 differentiation

Question 18

Tetracycline in children is contraindicated as it can lead to
A.	Grey skin colour
B.	Reyes syndrome
C.	Discoloured teeth
D.	Rash, vomiting and fever
E.	Liver damage

Answer 18

C. Discoloured teeth

Question 19

Which of the following statements about erythropoietin is false?
A. Recombinant EPO is licensed for anaemia in chronic renal failure
B. Receptors are homodimeric and situated on red blood cell precursors
C. Receptors on cardiac tissue indicate cardioprotective properties
D. At normal oxygen levels HIF 1 alpha is not hydroxylated so EPO transcription does not occur
E. Inability to produce EPO is linked with reduced exercise capacity

Answer 19

D. At normal oxygen levels HIF 1 alpha is not hydroxylated so EPO transcription does not occur

Question 20

What effect does TNF alpha not have in rheumatoid arthritis
A. Cause bone erosion via osteoclasts
B. Causes cartilage destruction
C. Has a positive feedback effect of inflammatory cytokines
D. Increases the chance of activating latent TB
E. Causes loss of muscle mass (sarcopenia)

Answer 20

D. Increases the chance of activating latent TB

Question 21

Which of the following is not an effect of fluid overload from chronic kidney disease
A.	Hyponatraemia
B.	Hypernatraemia
C.	Pulmonary oedema
D.	Pitting oedema
E.	Hypertension

Answer 21

B. Hypernatraemia

Question 22

Which one of the following describes oral allergy syndrome?
A. High sensitisation to storage proteins within peanuts; high risk of anaphylaxis
B. Cross-reactivity with lipid transfer proteins in peanuts; moderate risk of systemic reactions
C. Cross-reactivity with ubiquitious and unstable plant proteins; tingling and itchiness only
(Normally confined to the lips mouth and throat)

Answer 22

C. Cross-reactivity with ubiquitious and unstable plant proteins; tingling and itchiness only

Question 23

What is the function of Th2 cytokines in type 1 hypersensitivity?

a) To help bind IgM to bind to neutrophils
b) Class switch to IgE
c) To allow B cells to produce histamine
d) To send signals for mast cells to degranulate

Answer 23

b) Class switch to IgE

Question 24

Which drug treats autoimmune disease by blocking pathways involved in nucleotide synthesis?
A. Azathioprine
B. Prednisone
C. Colchicine
D. Dapsone
E. Aspirin 
TPMPT activity

Answer 24

A. Azathioprine

Question 25

``` What diuretics can cause gout? A. Carbonic anhydrase inhibitor B. Aldosterone antagonist C. Thiazide and related diuretics D. Sodium channel blocker E. Loop diuretics ```

Answer 25

C. Thiazide and related diuretics

Question 26

``` which is least likely to cause AKI? A. Hypervolaemia B. Hypokalaemia C. Sepsis/infections D. Drugs E. BMI ```

Answer 26

A. hypervolaemia (fluid overload) B. Hypokalaemia (volume depletion = aki) C. Sepsis/infections (sepsis associated acute kidney injury) D. Drugs (diuretics and many more – aki) E. BMI (risk factor?)

Question 27

``` Which structures are present in the medullary region of the kidney? A) Loop of Henle and collecting ducts B) Loop of Henle and PCT C) PCT and glomeruli D) Glomeruli and DCT E) DCT, PCT, glomeruli and Loop of Henle ```

Answer 27

A but: Collecting ducts, loops of henle, vasa recta and the interstitium

Question 28

Regarding teratogenicity, which of the following statements is incorrect? a) The embryonic period, during which organogenesis takes place (1st trimester) is when a foetus is most at risk of teratogenic effects b) Hydralazine, Labetalol, and Nifedipine are the recommended first-line treatments for severe hypertension in pregnancy (pre-eclampsia) c) Ramipril and Lisinopril are the recommended first-line treatments for hypertension in pregnancy (methyldopa is used 1st line) d) Teratogenic drugs can affect growth and functional development or have toxic effects on tissues (fetotoxicity) in the 2nd and 3rd trimester e) Sodium Valproate is contraindicated in pregnancy as it causes birth defects such as spina bifida

Answer 28

c, methyldopa = 1st line

Question 29

What are the characteristics of metabolic acidosis? A) a high pH, high HCO3- and the loss of H+ ions and addition of HCO3- ions B) a high pH, low PaCO2 and the reduction of H+ ions C) a low pH, high HCO3- and the loss of H+ ions and reduction HCO3- ions D) a low pH, high PaCO2 and the addition of H+ ions (resp) E) a low pH, low HCO3- and the addition of H+ ions and reduction HCO3- ions

Answer 29

E) a low pH, low HCO3- and the addition of H+ ions and reduction HCO3- ions

Question 30

Which ONE of the following statements about anaemia is INCORRECT? A. Anaemia of chronic kidney disease can be mild microcytic anaemia B. Vitamin B12 deficiency can increase MCV C. Haemolytic anaemia can increase MCV D. Iron deficiency anaemia show increased MCV E. Coombs positive patient show fragmented red blood cells on blood film

Answer 30

D. Iron deficiency anaemia show increased MCV (microcytic) (coombs = you have antibodies that act against your red blood cells) (macrocytic anemia can be due to b12 or folate deficiency) Haemolytic – rbc destroyed faster than made Macrocytic anemia - body has large rbc and not enough rbc Microcytic – small, red blood cells characterized by low mcv (ida – most common cause)

Question 31

What the does the presence of IgM indicate: • Activation of b cells • A recent exposure has taken • An allergic rection is present • A reaction between mother and fetus across the placenta • Activation of memory cells

Answer 31

• A recent exposure has taken | IgM antibodies = detection technique for diseases

Question 32

How does renal failure cause oedema?

Answer 32

Renal odema is associated with renal sodium retention.

Question 33

CKD impairs excretory renal function. What occurs if excretory function of kidney fails. A- Decrease in nitrogenous waste B- Increase in absorption of urate (increased retention serum uric acid that occurs as gfr decreases, slow down in the removal of uric acid from the body) C-Retention of phosphate D- Increase in creatinine release through urine

Answer 33

C-Retention of phosphate - Normal working kidneys can remove extra phosphorus in your blood, in CKD this cannot occur. Extra phosphorus puls calcium into bones

Question 34

What is desmopressin and whats its role?

Answer 34

Analogue of vasopressin (ADH) released from the anterior pituitary Limits hm water eliminated at the kidney (an antidiuretic!) ```  When bound to V2 receptors in the kidney it: Increased tubular water permeability Enhances water reabsorption Extracellular fluid = more dilute Urine = more concentrated ```

Question 35

desmopressin is a selective V2 receptor agonist... but it doesnt cause unwanted vasoconstriction- why?

Answer 35

Selective V2 receptor agonist – retains the antidiuretic activity of vasopressin but lacks the pressor activity so doesn’t cause the unwanted vasoconstriction

Question 36

what does desmopressin do when bound to V2 (ADH) receptors in the kidney? affect?

Answer 36

Increased tubular water permeability Enhances water reabsorption Extracellular fluid = more dilute Urine = more concentrated

Question 37

Does ADH promote dehydration?

Answer 37

when DEHYDRATED... ADH reduces water loss via lowered urine volume. Extracellular dehydration (hypovolaemia) stimulates specific vascular receptors that signal brain centres to initiate drinking and ADH release.

Question 38

what stimulates specific vascular receptors that signal brain centres to initiate drinking and ADH release?

Answer 38

hypovolaemia (extracellular dehydration)

Question 39

licensed indications of vasopressin? (BNF uses)

Answer 39

Diabetes insipidus (treatment or diagnosis) Primary nocturnal enuresis Post-op polyuria or polydipsia Polyuria or polydipsia after hypophysectomy Idiopathic nocturnal polyuria Nocturia associated with MS Renal function testing Mild to moderate haemophilia and von Willebrand’s disease Fibrinolytic response testing Lumbar puncture associated headache

Question 40

how can head injury cause Diabetes insipidus?

Answer 40

problems with ADH/ vasopressin (AVP) AVP is produced by the hypothalamus and stored in the pituitary gland until needed thus cause = PITUITARY TUMOUR form head injury or surgery damage

Question 41

what can affect V2 (vasopressin/ ADH) receptor function?

Answer 41

gene mutation

Question 42

what does desmopressin act on to increase expressino of what?

Answer 42

Acts on V2 receptors Increases expression of aquaporins More water reasoned into interstitium of kidneys

Question 43

what happens if lack of vasopressin/ ADH

Answer 43

ADH released when dehydrates, says 'bring back water!'- reabsorb cannot signal kidneys so its all flushed out in urine Desmopressin conserves some water so its not all flushed out. Only to small amount, large amount would lead to water intoxication. = =kidneys may excrete too much water. This causes frequent urination and can lead to dehydration, as well as low BP diabetes insipidus!!

Question 44

*** what do vasopressin and analogues promote? and whats their affect * * *

Answer 44

: Regularly release ADH: promote insertion of water channel proteins (AQP2) into apical membranes of cells in renal collecting ducts. Cells now have increased permeability to water, more water reabsorbed. Less water lost in urine.

Question 45

Differentiation between DI and nephrogenic diabetes insipidus?

Answer 45

DI: body doesn’t produce Vasopressin Nephrogenic diabetes insipidus: body produces Vasopressin but kidneys aren’t responding to it. (like T1/2DM)

Question 46

what is the difference between the two molecules and how does this affect their pharmacology desmopressin + vasopressin

Answer 46

VP: - (Only available as solution for injection) - More selective for V2 receptors on collecting duct = more potent. Therefore less vasoconstrictive effect - Short half life- administered every 4 hours. - Rapid elimination - Can’t use IV not licensed for use in DI patients anyway. - 3 vasopressin receptors: v1,V2,V2. All have diff functions.

Question 47

what the desmopressin is for, how it works and why he needs to use it for DI?

Answer 47

DI = polydipsia and polyuria (extreme thirst and frequent urination). - Not enough ADH in body (role of dec urine production) so must be given as medication. - Desmopressin: more powerful than endogenous ADH, stop kidneys producing urine. - Regulates water in body and alters hm brought back from kidney

Question 48

what would happen if patient stops takinig desmopressin for DI. (hint- serum and urine osmolality changes)?

Answer 48

Apical memb. ADH ↑ aquaporins on memb so ↑ water can get through and be absorbed Basolateral: always has aquaporins V1: smooth muscle contraction in cardiovascular system V3: promote ACh release via this receptor Calculated osmolality = 2 x serum sodium + serum glucose + serum urea (all in mmol/L). Uosm = 1.25 × urea (mmol/l) Dilute, pale urine Become more thirsty Serum osmolality: ↑ as serum Na ↑ More mols in blood = ↑ serum osmolliy. ↑ water in blood = lower serum osmolality Urine osmolality ↑ Other symptoms: Fatigue, anorexia, weight loss

Question 49

ADH effects and drugs: NSAIDs, Li, ethanol?

Answer 49

NSAIDs: Naproxen, carbamazepine: used for seizures. Increase action of ADH- urine more concentrated Li: for bipolar disorder. Inhibits ADH. More dilute urine produced Ethanol inhibits secretion of ADH

Question 50

osmolality and osmolarity units?

Answer 50

Osmolarity: mmol/L easier to measure. As sample given in ml and L Osmolality: mmol/kg more accurate

Question 51

why should patient with DI not drink excessively/ drink lots of mineral energy drinks?

Answer 51

Should be guided by thirst else: hyponatraemia - reduction in conc of Na in blood. More water retention

Question 52

Homeostasis is achieved through the process of what?

Answer 52

glomerular filtration of plasma to produce an ultrafiltrate. The tubules then process this ultrafiltrate so that the final urine flow rate and solute excretion meet the homeostatic needs of the body. In the steady state, our total body water content and salt content remain constant. An increase or decrease in water and salt intake is paralleled by an equivalent change in renal water and salt excretion.

Question 53

Osmolality and osmolarity are measurements of ?

Answer 53

solute concentration of a solution. In practice, there is negligible difference between the absolute values of the different measurements.

Question 54

Calculated osmolarity equation

Answer 54

= 2 (Na+) + 2 (K+) + Glucose + Urea | (all in mmol/L);

Question 55

Mrs Brown’s calculated osmolality = (2 x 118) + (4.9 x 2) + 4.6 + 4.8 = 255mOsm/l comment on the value

Answer 55

Normal is around 285 ! Or serum Na x 2 + serum potassium x 2 + urea + glucose All in mmol/L

Question 56

plasma osmolality is a guide to | intracellular osmolality. why?

Answer 56

cell membranes in general are freely permeable to water, the osmolality of the extracellular fluid (ECF) is approximately equal to that of the intracellular fluid (ICF).

Question 57

In normal people, increased osmolality in the blood will stimulate secretion of what?

Answer 57

ADH -> inc water reabsorption, more conc urine, less conc blood plasma

Question 58

elevation of ADH may be associated with what?

Answer 58

stroke mortality -- associated w DI

Question 59

possible causes of: normal/high serum osmolality high urine osmolality (conc)

Answer 59

* Dehydration * Renal disease and uraemia * Congestive heart failure * Addison's disease * Hypercalcaemia * Diabetes mellitus/hyperglycaemia * Hypernatraemia * Alcohol ingestion * Mannitol therapy

Question 60

possible causes of: normal/high serum osmolality low urine osmolality (dilute)

Answer 60

DI !

Question 61

possible causes of: LOW serum osmolality HIGH urine osmolality (conc)

Answer 61

Syndrome of inappropriate ADH secretion | SIADH

Question 62

possible causes of: LOW serum osmolality LOW urine osmolality - w no inc in fluid intake (dilute)

Answer 62

-Overhydration •Hyponatraemia •Adrenocortical insufficiency •Sodium loss (diuretic or a low-salt diet)

Question 63

whats urine osmolality in dehydration?

Answer 63

very high as very conc! | 800-1400mOsm/kg

Question 64

whats SIADH?

Answer 64

syndrome of inapp ADH secrtn Inappropriately concentrated urine in the setting of a low plasma osmolality – inappropriate ADH production and release (TOO MUCH!)

Question 65

SIADH causes

Answer 65

Brain and spinal cord conditions, such as a direct injury, infection, or fluid buildup  Cancer  Lung conditions, such as COPD, pneumonia, or tuberculosis  Drugs: usually those used to treat diabetes, cancer, or depression  Family history of SIADH  Too much physical pain or stress on your body

Question 66

1How would investigating the urine help confirm if SIADH happening?

Answer 66

Urine would be in little volumes and more concentrated as ADH inhibits urine production. Check for urinary sodium excretion >30mmol/L

Question 67

SIADH Symptoms

Answer 67

 Tiredness and weakness  Muscle pain, cramps, or headaches  Dark urine or changes in how much urine is produced  Decreased appetite for food, or increased thirst  Diarrhea or constipation  Nausea or vomiting  Seizures  Trouble thinking clearly, or hallucinations

Question 68

What to do. about SIADH?

Answer 68

1. Investigate the cause (more bloods, chest x-ray, CT scan, check drug history) 2. Can be corrected with an AHD V2 receptor ANTAGONIST “vaptans” = Tolvaptan

Question 69

common feauture of SIADH?

Answer 69

very low urine osmolality! e.g. 180 should be 500-850

Question 70

What medical conditions and medications can lead to overproduction ADH hormone?

Answer 70

(SIADH) T2DM drugs, antidepressants, brain injury, brain infection, brain abscesses, subarachnoid hemorrhage Epilepsy head trauma infections autoimmune… Cancers Lung disease

Question 71

whichi drugs best to treat SIADH: increase excretion of free water whilst minimising excretion of sodium into urine= correct serum sodium concentration and serum osmolality. ?

Answer 71

Diuretics help rid your body of salt (sodium) and water. Most of these medicines help your kidneys release more sodium into your urine. The sodium helps remove water from your blood, decreasing the amount of fluid flowing through your veins and arteries. Fluid restriction recommended V2 receptor antagonist !! VAPTAN selective for V2 receptors

Question 72

monitoring with VAPTAN for SIADH?

Answer 72

Serum sodium: measure every 6 hours after starting treatment for first 2 days. Renal function test check again

Question 73

acid base and angiotensin system SGT What standards should you meet if you are offering to check peoples blood pressure?

Answer 73

``` Relaxed setting adequate training and reviews equipment regularly calibrated and maintained cuffs should be appropriate tablets ask for consent ```

Question 74

what BP checks to do on elderly?

Answer 74

sitting and standing BP to check for postural hy[ptension: risk of falls

Question 75

What should you check on patients before taking their bp and why?

Answer 75

Pulse to check for irregularities in heartbeat/ flutter due to AF

Question 76

What stage of hypertension is a reading of 162/101?

Answer 76

stage 2

Question 77

What may be offered to confirm a diagnosis of hypertension without risk of white coat syndrome?

Answer 77

ABPM

Question 78

what to offer t patietn diagnosed with stage 2 hypertension?

Answer 78

``` antihypertensives (diuretics spec thiazide d - bendroflumethiazide etc) lifestyle advice: - dietary salt - alcohol consumption - physical activity - mental health ```

Question 79

Patients with suspected hypertension must also be investigated for target organ damage. What might an ECG be used to see the development of?

Answer 79

AF

Question 80

additional tests for stagge 2 hypertension?

Answer 80

target organ damage hypertensive retinopathy LV hypertrophy on ECG blood tests: serum elec, creat, eGFR, fasting gluc and lipids, Na, K in urea urinalysis for proteins. may cause kidney damage blood gluc leveks: HbA1c

Question 81

What tool may be used to assessed CVS risk?

Answer 81

QRISK3

Question 82

What non-pharmacological and dietary advice to stage 2 hypertensive patieht

Answer 82

Control + improve diet -reduce risk of heart problems: • e.g. use wholegrain bread, and brown rice. • min 5 portions fruit + veg a day. • low-fat foods - avoid lot of fat and sugar. • Reduce excessive caffeine consumption, low dietary sodium intake (reduce or substitute any sodium salt). • Cut alcohol intake. • Avoid some exercises: sprinting/ weightlifting as they raise your blood pressure rapidly and put strain on heart and blood vessels Decreasing salt intake decreases BP • Less Na, K, Cl ions in ascending LoH • No reabsorption into medullary interstitium • Prevent cortico-medullary gradient forming • More urine produced, decreased Na reabsorption so more excreted, • Blood volume and pressure decreased. Caffeine: stimulant increases HR and maybe anxiety. Check how much he drinks Signpost local support networks

Question 83

whats BP regulated by?

Answer 83

BP regulated by macula densa of DCT and afferent arteriole = juxtaglomerular apparatus.

Question 84

Why might a Hb1ac test be carried out in patients with hypertension?

Answer 84

Average blood glucose of last 2-3 months, check if patient is diabetic, shows how much sugar has glycosylated in this peroid

Question 85

How would you physiologically explain the rationale behind the dietry advice regarding dec salt intake?

Answer 85

increased salt means body retains water increases plasma volume puts pressure on blood vessels can worsen bp

Question 86

What drug and class would be recommended to a white man under the age of 55 diagnosed with hypertension? 1st line what if this is not well tolerated?

Answer 86

ACEi such as ramipril look at most cost effective one and ones with best patient compliance (OD) or ARB if ACE not tolerated. DO NOT COMBINE

Question 87

why ACEi first line in hypertension (most of the time)

Answer 87

Reduce blood pressure by relaxing blood vessels. Usually first line and inhibit RAAS. .... Potent stimulation of Na reabsorption from PCT so blood volume hence BP increased. Opposite true for the drugs. Renin release inhibited so less ACE enzyme levels in body, decreased BP.

Question 88

What side effects would you warn patients starting Acei about?

Answer 88

- common: dry cough, if excessive refer back to GP, swap to ARB - angioedema so look for swelling of lip and throat take first dose at night to reduce first dose hypotension until bp stabilised and then go to morning dose - hyperkalaemia (excess K levels in blood arrythmias) monitor after 2 weeks- blood test for kidney function and can see K levels, fatigue, dizziness as lower BP (hypotension), headaches, loss taste. Diarrhoea- nausea and vomiting- become dehydrated Reduce arteriolar- vasoconstriction Don’t stand up very quickly etc as may feel dizzy and have falls. Get up out of bed- sit on bed for a bit

Question 89

Why may a dry cough develop in patients who are on Acei?

Answer 89

ACE breaks down bradykinins in lungs If inhibited these accumulate hence cough develops

Question 90

Outline how Acei such as captopril work?

Answer 90

Inhibit the ACE enzyme Ang I cannot be converted to ang II Blocks release of aldosterone causing vasodilation and relax of blood vessels and water loss therefore reduces blood vol and blood pressure better blood flow through kidneys

Question 91

Acei retain potassium which can lead to the risk of developing?

Answer 91

hyperkalaemia

Question 92

What monitoring is required with Acei?

Answer 92

Renal function and electrolytes (Na/Cl) before and 2 weeks after starting every 3-6 months thereafter as May cause frop in renal perfusion pressure thus drop in (GFR), renal failure possible. Also increase creatinine levels

Question 93

Why is monitoring needed for Acei and what could be the consequences if this isnt done?

Answer 93

Lowering BP affects renal perfusion potential to cause renal impairment and failure Acei can worsen hyperkalaemia and renal failure hence want to monitor mild consequneces can be nausea severe can lead to arrythmia and cardiac arrest

Question 94

Diarrhoea and vomiting in patients taking Acei may mean dehydration and worsening of renal impairment. What would you recommend the patient to do?

Answer 94

Stop taking the acei for a few days

Question 95

Which other classes of drug inhibit activity of the renin-angiotensin system other than ACEi?

Answer 95

ARBs (Ang II rec blockers) renin inhibitors aldosterone rec antagonists

Question 96

How do ARBS inhibit the RAS system?

Answer 96

Angiotensin receptor blockers prevent the binding of ang II at the site

Question 97

Why do patients on Acei no longer get a dry cough when switched to ARBS?

Answer 97

bradykinins continue to be broken down therefore are not accumulating

Question 98

What do renin inhibitors do?

Answer 98

Prevent the conversion of angiotensinogen to angiotensin I

Question 99

Why are some populations not recommended acei as first line?

Answer 99

Afro carribean populations recommedend CCBs instead as they dont respond well to ACEi and are at a higher risk of angioedema

Question 100

What metabolic abnormality is demonstrated by these results: pH - 7.09 PaCO2 - 3.6 kpa PaO2 - 15 kpa HCO3 - 8mmol/L

Answer 100

metabolic acidosis pH - 7.09 low PaCO2 - 3.6 kpa too low PaO2 - 15 kpa acceptable HCO3 - 8mmol/L too low

Question 101

What is the normal range for bicarbonate in the blood?

Answer 101

22-26 mmol/l

Question 102

clinical consequences is metabolic acidosis left untreated?

Answer 102

Death and organ failure. esp of have impaired kidney function anyway

Question 103

Why might patients experincing metabolic acidosis also experience breathlessness?

Answer 103

trying to blow out in an attempt to raise pH to normal OR Breathlessness may be due to heart attack- blood can’t travel to tissues quick. Low CO2 in response to that

Question 104

What are clinical consequences if metabolic acidosis is left uncorrected?

Answer 104

Causes insulin resistance leading to diabetes decreased cardiac output leading to hypotension Altered oxygen delivery decreased atp production denaturing of enzymes leading to organ failure

Question 105

When sodium bicarbonate is given to restore the serum bicarbonate levels, why is the increase in small increments?

Answer 105

to prevent levels going to high

Question 106

Sodium bicarbonate replacement q If the volume of distribution of HCO3- is approximately 0.5 mmol/kg body weight and Mrs Begum weighs 70kg how much sodium bicarbonate does the team need to give Mrs Begum to restore the serum bicarbonate to 24 mmol/L? (currently: 8mmol/L)

Answer 106

Bicarbonate deficit = Vd x weight (kg) x (bicarb range you want – actual) = 0.5 x 70kg x (24-8) = 560mmol NB: Is an approximation! BNF Products: 1) 1.26% Sodium bicarb 500ml 2) 8.4% Sodium bicarb 200ml 1.26g in 100ml (11.9/1 x 1.26 = 15mmol in 100ml) 12.6g in 1000ml = 150mmol in 1L 600mmol in 4L Nearly 4l required of 1.26%, high risk in patient with MI as a lot of Na and big volume Less volume with 8.4% but very hyperosmolar!!!!

Question 107

know the dangers and precautions if infusing 8.4% bicarbonate and as with all treatment, the monitoring parameters and consequences of over correction.

Answer 107

8.4% only need 500mL roughly. But very potent. Into small veins. Alkaline, necrotic, inflammation Should be put into central vein not peripheral. monitor (ongoing) - ABG analysis: minimise possibility of overdose and alkalosis - Serum electrolytes: replacement of Ca, Cl, L important if alkalosis occurs. Too rapid correction of Na = severe neurological effects. - Fluid balance: excess Na retained, extracellular fluid excess may be retained, peripheral oedema - Acid base balance: bicarbonate induced metabolic alkalosis can occur. Na is associated with chloride and bicarbonate in the regulation of acid–base balance. Na Ca K pH

Question 108

difference between HCO3 in - resp alkalosis - metab alkalosis?

Answer 108

- LOW | - HIGH

Question 109

SGT: Reduced Renal Clearance | whats morphine and how does it work?

Answer 109

: strong painkiller, works by blocking signals from travelling along nerves to the brain. Common side effects: constipation, feeling sick and sleepiness. Can become addicted to morphine if treatment not properly reviewed.

Question 110

What are the usual adverse effects of morphine?

Answer 110

Morphine is an opioid, effects are related to agonist activity at mu receptors: expect drowsiness, dizziness, spiritual depression, dry mouth, nausea, vomiting, confusion, flushing, constipation. For all opioids, adrenocortical insufficiency possible: reduce dose. Expect constipation: occurs via stimulation of mu-opioid receptors on myenteric plexus, inhibits gastric emptying and reduces peristalsis. Should prescribe stimulant laxative with this. Reduced GI motility = com=nstipation Other side effects include: Serious allergic reaction which causes difficulty in breathing or dizziness; swelling of the eyelids, face or lips; rash or itching (especially affecting your whole body). If you are affected by these important side effects contact a doctor immediately. Respiratory depression CNS suppression Very common: may affect more than 1 in 10 people • feeling sick (nausea) • vomiting • shallow breathing • constipation • sleepiness • not knowing where you are (disorientation) • sweating • a perception of seeing or hearing things (hallucinations) • uncomfortable mood • feeling of very intensive happiness and wellbeing (euphoria) • tolerance and dependence (with long-term treatment)

Question 111

What are the usual adverse effects of morphine?

Answer 111

opioid, effects related to agonist activity at mu receptors: drowsiness, dizziness, spiritual depression, dry mouth, nausea, vomiting, confusion, flushing, constipation. For all opioids, adrenocortical insufficiency possible: reduce dose. Other side effects include: Serious allergic reaction which causes difficulty in breathing or dizziness; swelling of the eyelids, face or lips; rash or itching (especially affecting your whole body). If you are affected by these important side effects contact a doctor immediately. Respiratory depression CNS suppression Very common: may affect more than 1 in 10 people • feeling sick (nausea) • vomiting • shallow breathing • constipation • sleepiness • not knowing where you are (disorientation) • sweating • a perception of seeing or hearing things (hallucinations) • uncomfortable mood • feeling of very intensive happiness and wellbeing (euphoria) • tolerance and dependence (with long-term treatment)

Question 112

common side effecr of morphine and what may be prescribed alongside?

Answer 112

constipation: occurs via stimulation of mu-opioid receptors on myenteric plexus, inhibits gastric emptying and reduces peristalsis. Should prescribe stimulant laxative with this. Reduced GI motility = constipation

Question 113

morphine metabolism and clearance from body?

Answer 113

``` Excreted renally (10%) Metabolised to codeine and glucose indies (3 and 6) in liver ``` Also metab to Normorphine Metabolite: M6G contributes most to analgesic effect M3G and M6G cleared by kidneys Poor oral bioavailability 15-64% very variable

Question 114

If half-life of morphine is unchanged in renal failure why is patient exhibiting severe signs of opiate toxicity? ( clearance of the different morphine metabolites and pharmacological properties)

Answer 114

• Dose too high? Calculate using dose adjustment table • Extreme caution with all opiates in patients with impaired renal function • Potential accumulation of M6G (active metabolite, more potent than morphine) and M3G. • Half life of M6G increased from 3-5 hours in normal renal function to about 50 hours in ERF (established renal failure) Caused by respiratory depression: .. Due to accumulation of metabolites M6G: high affinity for opioid receptors High Half life = accumulate and toxicity

Question 115

drug for OD of morphine in reduced renal clearance?

Answer 115

Naloxone (opioid receptor antagonist, for acute opioid overdose–high-dose regimen [when rapid titration with naloxone is necessary to reverse potentially life-threatening effects]) readily available: initially 100mcg-200mcg then 100mcg up to 2 doses at 1 minute intervals. Rapidly reverses opioid overdose. Attaches to opioid receptors and reverses and blocks effects of other opioids. Will cause an increase in mean aortic pressure, cardiac output. rapidly absorbed after oral administration, but this route may not be ideal due to high metabolism (pre-systemic). Given IV/ IM Start at 400mcg, can go up to 2mg M6G 10-15 hours half life Naloxone: 1-1.5 hours half life (SPC!!) Therefore have to administer naloxone multiple times to prevent effect wearing off and opioid toxicity coming back.

Question 116

how is morphine excreted?

Answer 116

renally: thus has those side effects consider patient eGFR and titrate

Question 117

Safest opioids in patients with renal failure

Answer 117

Fentanyl, - not renally excreted - transdermal patch - BUT time takes to titrate dose etc... not best option hydrocodone, - renal exc - half life prolonged in renal failure Tramadol: Excreted renally, not strong enough (not pure opioid analgesic) wont have best effects Methadone: Used to help treat addictions Fewer SEs and active forms than morphine Must be admin by specialist for pain due to pharmacokinetics

Question 118

consequences of inapp dose of aciclovir in immunocomp patient?

Answer 118

Acute kidney injury Or increased risk of adverse effects Has to maintain adequate hydration: to reduce renal complications. Aciclovir excreted in urine unchanged = crystals in urine, want to avoid

Question 119

SGT: Calcium and Phosphate normal phosphate levels in dialysis?

Answer 119

0. 8 – 1.5 mmol/L normal | 1. 1 - 1.7mmol/L dialysis: higher as less effective than kidneys, difficult to correct to normal artificially.

Question 120

whats phosphate needed for? (4)

Answer 120

Phosphate is a charged ion containing the mineral phosphorous. This mineral is needed by the body to build and repair bones and teeth, help nerves function, and make muscles contract. Needed for: • Muscle function • Heart (cardiac) function • Bone metabolism • Cellular functions: energy metabolism and cell signalling

Question 121

why is parathyroid gland likely to be overactive if phosphate is high?

Answer 121

Kidneys not excreting phosphate, so goes up, PTH increases too PTH want to get rid of more but can’t as kidneys not working properly. PTH trying to mobilise Ca and phosphate too as a result. PTH increases osteoclast activity to increase serum Ca

Question 122

role of Ca phosphate binders? commonly sevelamer and lanthanum

Answer 122

suppress parathyroid hormone concentrations PTH regulates levels of calcium and phosphate in blood, work by homeostasis and both are regulated by pathways involving vitamin D. Calcium given to increase calcium levels, therefore decrease phosphate levels back to normal.

Question 123

non-pharmacological measures to reduce serum phosphate concentration

Answer 123

Renal dietician:... Milk, red meat, dairy, grains, legumes, chocolate, beer Difficult to avoid

Question 124

difference in vitamin D in multivitamin and the alfacalcidol | vitamin revision in general

Answer 124

Alfacalcidol: given in active form (kidney cant currently convert so multivitamin) Vit D, K, A(too much is toxic) fat soluble Water soluble vitamins (C) just get excreted, not stored Vit K needed for clotting factors Need afacalcidolin hydroxylated form to be active. Supplement with water soluble vitamins not fat soluble

Question 125

possible adverse effects of taking both calcium acetate and alfacalcidol what to monitor?

Answer 125

Hypercalcaemia!! monitor plasma calcium concentration, check weekly/fortnightly intervals. Constipation, anorexia, levels increase, more nausea vomiting… delirium, coma 2.6: levels getting high Higher than 3: needs immediate treatment At risk: renal patients Malignant matasticies (bone) Also monitor phosphate!

Question 126

hypercalcaemia causes

Answer 126

result of overactive parathyroid glands. | cancer, certain other medical disorders, some medications, and taking too much of calcium and vitamin D supplements.

Question 127

What is cinacalcet and how does it reduce overactivity of parathyro?

Answer 127

Bone resorption inhibitor drug- lowers PTH, -> decrease in serum Ca concs, improve hyperparathyroidism problem Increase sensitivity of Ca receptors. Reduce PTH released. Secondary Hyperpara (as caused by renal)

Question 128

What are the potential serious side effects of taking cinacalcet

Answer 128

Hypocalcaemia: paresthesia, muscle spasms, cramps, tetany, circumoral numbness, and seizures. Can also prolong QT interval, more risk of ventricular arrhythmias (so do some drugs- methadone)

Question 129

monitoring with cinacalet? hypocalcaemia

Answer 129

serum-Ca conc before initiation of treatment and within 1 week after starting treatment or adjusting dose, then monthly thereafter. PTH conc 1–4 weeks after starting treatment or adjusting dose, then every 1–3 months. Want it to decrease. May decide after those months that its not working well, stop drug as don’t want to cause AD effects, expensive treatment Phosphate : in reasonable range

Question 130

SGT 9: UTI classic symptoms of UTI +and what else in elderly?

Answer 130

elderly: confusion and lethargy rather than the classic symptoms

Question 131

likeliest causes of pain passing urine (also called dysuria)

Answer 131

Infection or inflammation of bladder and/or urethra (cystitis) UTI: lower (bladder) and upper (kidneys, more serious can get systemic) STI may also cause- if passing urine over inflamed area = stinging Vaginitis: inflammation of mucus membranes also caused by yeast infections.

Question 132

qs to ask UTI patient?

Answer 132

* Experienced any other symptoms such as urinary frequency/urgency, lower abdominal pain, polyuria. Haematuria, fever/chills * Can ask her if she’s pregnant, has any kidney problems e.g. kidney stones

Question 133

What first line antibiotic treatment is recommended for UTI?

Answer 133

Nitrofurantoin: if estimated glomerular filtration rate (eGFR) ≥45 ml/minute 100 mg modified-release twice a day for 5 days (or if unavailable, 50 mg four times a day) for 3 days Trimethoprim: if low risk of resistance 200 mg twice a day for 3 days (NICE)

Question 134

why does cystitis need antibiotics?

Answer 134

caused by bacteria (germs) from gut getting into your bladder (also called lower UTI). Sometimes symptoms improve by themselves, but many people will need antibiotic treatment

Question 135

risks and benefits potential, of antibiotics for UTI?

Answer 135

Potential risks CommonSE: nausea, diarrhea, and stomach pain. Sometimes these symptoms can lead to dehydration and other problems Risk of not taking the antibiotics course: Infection may recur, and will be more difficult to treat when it does. Potential benefits Reduced chances of infection. Prevents Disease Progression (getting severe and complicated).

Question 136

Who does need to see a GP with urinary infection symptoms

Answer 136

Pregnant with symptoms of a UTI. If caring for an older, frail person who may have a UTI. If you have symptoms of a UTI after surgery. your symptoms get worse or do not improve within 2 days. (NHS)

Question 137

How does potassium citrate work (cystitis)

Answer 137

Makes the urine more alkaline by increasing the pH. This would ease symptoms such as pain or burning sensation during urination, and pain in lower belly.

Question 138

can potassium citrate be used in patients on nitrofurantoin?

Answer 138

no as potassium citrate will cause it to work less well and should not be used whilst on these antibiotics

Question 139

what patients should not have potassium salts?

Answer 139

Patients with reduced renal function should not have potassium salts, or those taking potassium sparing medication NICE does not recommend the use of alkalinsing agents to treat UTI symptoms. Potassium citrate is not antibacterial.

Question 140

why there is an increased chance of antibiotic resistance in nursing homes

Answer 140

Patients in nursing homes often have health conditions that can weaken their immune system, and they're often on prolonged antibiotic use, which contributes to antibiotic-resistance.

Question 141

NICE: Preventative measures of UTI?

Answer 141

* not using perfumed bubble bath, soap or talcum powder around your genitals (use plain unperfumed varieties) * having a shower, rather than a bath (this avoids exposing your genitals to the chemicals in your cleaning products for too long) * going to the toilet as soon as you need to pee and always emptying your bladder fully * staying well hydrated (drinking plenty of fluids may help to stop bacteria multiplying in your bladder) * always wiping your bottom from front to back when you go to the toilet * emptying your bladder as soon as possible after having sex * not using a diaphragm for contraception (you may wish to use another method of contraception instead) * wearing underwear made from cotton, rather than synthetic material, such as nylon, and not wearing tight jeans and trousers

Question 142

SGT: Drugs and Acute Kidney Injury furosemide 40mg once daily, indication?

Answer 142

loop diuretic for oedema/symptoms of heart failure. Not first line forresistant hypertension

Question 143

why would HR go to 110 up in BP 85/40?

Answer 143

BP low so heart treis compensating. to help organ perfusion

Question 144

urinalysis results: | blood +++, protein +++, leucocytes ++ and nitrites ++.

Answer 144

Nitrites and leukocytes increased by UTI

Question 145

risk factors for developing acute kidney injury

Answer 145

``` Hypertension, diabetes,NSAID/ACEI/ARB use Over 65. Ibuprofen and Ramipril. Nephrotoxic Currently hypotensive Dehydration, furosemide Been vomiting= extra losses Fever: symptom of systemic infection. Sepsis. Also further losses through sweating. ```

Question 146

whats pyonephrosis? and cause

Answer 146

pus in the renal pelvis—results from urinary tract obstruction in the presence of pyelonephritis.... cause: Kidney infections (pyelonephritis) typically happen when bacteria is not flushed out of the body with urine.

Question 147

interventions about meds to make on patient w UTI | - sgt

Answer 147

Stop ibuprofen, replace with paracetamol Withhold furosemide (making dehydration worse) and Ramipril Ask when she has pain: if ibuprofen and paracetamol PRN. May not need them both Ramipril dilates efferent arteriole, drop in BP to kidneys as no pressure build up across kidneys. NSAIDs: COX inhib- inhibit prostaglandin production from phospholipids etc. Can check previous prescriptions but ask patient when she takes it. Lactic acidosis controversial issue with metformin in patients with renal failure. Usually stopped for short time while patient unwell.

Question 148

empirical antibiotic therapy:What national guidelines exist to guide the choice of antibiotic and what is the recommendation?

Answer 148

Empirical: best guess Cephalexin/co-amoxiclav/-fluoxetine/Trimethoprim Short course: 7-14 days for therapy If had penicillin allergy, wouldn’t give co-amoxicillin Cephalexin: cephasporin- similar chemical structure to penicillin. Cross-sensitivity likely Floxacins: antibiotics- change gut flora. Causes overgrowth of C.Diff. Have to be confident with choice if given. And these antibiotics change gut flora IV route preferred originally as he is vomiting Gentamicin Narrow therapeutic range and has 2 major toxicities: Ototoxic (ears) and Nephtoxic (kidneys) Alicasin

Question 149

likely cause of decreased glucose?

Answer 149

vomiting, been excreting

Question 150

Prerenal AKI symptoms?

Answer 150

Prerenal as drugs, fever, vomiting, and has hypotension. Perfusion failure in kidneys Creatinine: estimation of muscle, so different or elderly

Question 151

most appropriate drug to control Mrs Brown's blood glucose concentration (low bg)

Answer 151

Short acting/soluble insulin and titrate | Repeat or IV infusions

Question 152

what decisions to make when presc antibiotic in renal failure, for UTI?

Answer 152

estimate of creatinine clearance or eGFR to make these decisions also dosing and monitoring of gentamicin in reduced renal clearance

Question 153

what antibiotic to avoid in eGFR below 45? and what to recommend? monitoring?

Answer 153

Nitrofurantoin :Increased risk of neuropathy Trimethoprim used. IV formulation not availble only oral. Can cause hyperkalaemia, K already high. Not used in serious infection Only nephrotoxic gentamicin left. Would take blood tests before each dose so you have trough level. 80mg BD. Do blood tests before 8pm night dose to ensure trough level: gentamicin level of 5-10mg/L therapeutic dose. WANT TROUGH TO COME BELOW 2, to prevent serum going over 10.

Question 154

whats drugs to treat hypertension, esp in T2DM?

Answer 154

ACE inhibitors may wish to discuss 'sick day rules'- think kidneys website CPPE Think Kidneys https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2015/03/Pharmacists-Thinking-Kidneys.pdf Think Kidneys statement on wide use of sick day rules https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2020/01/2020-AKI-Sick-Day-Guidance-Think-Kidneys.pdf

Question 155

SGT Chronic Kidney Disease and Hyperkalaemia CKD is classified using what?

Answer 155

using the eGFR and ACR categories, and the different categories from NICE guidance

Question 156

What is chronic kidney disease?

Answer 156

The gradual loss of kidney function. Affects waste and excess fluids filtered from blood into urine for excretion, build up could be toxic. Irreversible Could be from reduced kidney function/ structural changes

Question 157

hows CKD diagnosed?

Answer 157

``` Diagnosis: • Incidental raised serum creatinine • proteinuria of more than 3mg/mmol • persistent haematuria • urine sediment abnormalities ``` ``` may be asymptomatic in early stages NICE: egfr can be normal but may be structural changes e.g. high protein in urine. Egfr can still be normal Changes must be present for 3 months ACR more than 3mg/mmol (albumin:creatinine) in morning. ```

Question 158

CKD symptoms/ possible risk factors?

Answer 158

* General: lethargy, itch, breathlessness, cramps (often worse at night), sleep disturbance, bone pain, or loss of appetite, vomiting, weight loss, and taste disturbance (often present with end-stage disease). * Urine output, such as polyuria; oliguria; nocturia; or anuria (due to possible AKI, obstructive uropathy causing urinary retention; or end-stage renal disease). * Any potentially nephrotoxic drugs: OTC/herbal * Any associated co-morbidities or complications of CKD. * Any family history, such as autosomal dominant polycystic kidney disease. * Any associated clinical features of anxiety or depression.

Question 159

Why do people with type II diabetes get chronic kidney disease?

Answer 159

Kidneys filter blood and over time, high blood sugar from diabetes -> damage to the blood vessels + nephrons in kidneys and hinder their activity, causing kidney damage. Diabetic nephropathy !!! High bgc = blood vessels cant filter as well Also hypertensive. Microvascular complications. May also develop macrovascular complications.

Question 160

hows CKD in T2DM detected?

Answer 160

Detection • Creatinine levels • Proteinuria • eGFR: Clinical laboratories should report eGFR either as a whole number if it is 90 ml/min/1.73 m2 or less, or as 'greater than 90 ml/min/1.73 m2'. • Albumin in urine. ACR accurate representation.

Question 161

how would you know if kidney problem/ CKd is due to diabetes?

Answer 161

History consistent with developing. 8-10 years after diabetic diagnosis, and microvascular complications. Look at medical history. retinopathy, high BP, ACR over 100mg/mmol. Means must have had it for years as slow increase in ACR over long period of time. Blood in urine: haematuria. If patient is systematically ill eGFR worsened rapidly: characteristic of AKI, but gradual = CKD.

Question 162

what may be caused if a) eGFR worsened rapidly: b) worsened gradually?

Answer 162

eGFR worsened rapidly: characteristic of AKI, | but gradual = CKD.

Question 163

Which people with chronic kidney disease need to see a kidney specialist?

Answer 163

ACR above 70mg/mmpol OR 30mmol/ML with UTI/ something. ACR= abumin:creatinine ratio

Question 164

whys ramipril prescribed in CKD in diabetes for?

Answer 164

to prevent progression of CKD in diabetes rather than control blood pressure. ... ACEi and ARBs reduce proteinuria and prevent progression of CKD and should be used even if BP controlled. Treating proteinuria: associated with CKD. Hypertension. NICE. Titrate to highest dose they can tolerate. 3mg/mmol or more? If ACR above 70mg/mmol!!

Question 165

mointoring/ counselling before starting ramipril in CKD in diabetes ?

Answer 165

renal function and electrolytes BEFORE ACEi started. Or dose increased during treatment and more often if side effects experienced * BP regularly, serum electrolytes * First dose: may experience hypertension- sit down when taking. * ACEi could also precipitate AKI. May need to omit a dose or 2 if developed AKI

Question 166

how to stop CKD in T2DM getting worse?

Answer 166

• Smoking, alcohol, exercise. • Would help with diabetes and hypertension too. May also need dietician especially if . • Don’t take NSAIDs- could reduce eGFR, precipitate CKD. • Could also check his weight and BMi for normal range. • Waist-hip ratio. May have more fat there even if BMI normal • Cardiac risk assessment Can ask about his diet and lifestyle choices Measure proteins, creatinine, etc to check CKD is not advanced and requiring prompt treatment.

Question 167

his blood pressure is 65/30 and his pulse rate is 30 beats per minute. whats happened to patient?

Answer 167

Complete heart block, probably due to hyperkalaemia due to the ramipril.

Question 168

What is ventricular rate on ecg (descrobe main obsevrations)

Answer 168

P wave: atrial depolarisation: Atria contract QRS: vent depolarisation. Contract T wave: vents relax

Question 169

calculating the ventricular rhythm/ rate?

Answer 169

Count the number of large squares between the R peaks. There are 300 of the large squares per minute, so rate = 300/ no. of large squares. 300/11 (big boxes between 2 QRS complexes) =27bpm

Question 170

lack of QRS complexes means what?

Answer 170

Cant see P waves for some... Sinus node conducts elec first, goes to AV. Elec impulses should reach AV node then to vebtricles to contract. AV node not doing job properly as lack of QRS complexes (when ventricles contract). 3rd degree AV block, no communication between QRS and P.

Question 171

calcium gluconate effect on heart

Answer 171

For acute severe hyperkalaemia (low Calcium). • Increases Ca level s in blood through binding to excess potassium/Mg * Calcium antagonizes the cardiotoxicity of hyperkalemia by stabilizing the cardiac cell membrane against undesirable depolarization. * Onset of effect is rapid (≤ 15 minutes) but relatively short-lived.

Question 172

Bnf management of hyperkalemia under fluid and electrolytes

Answer 172

Slow IV injection over 3-10mins. Immediate effect but only lasts few mins? SPC!! If admin too rapidly: nausea, vomiting, hot flushes.

Question 173

How much glucose and insulin (and what type of insulin) would be appropriate in CKD?

Answer 173

Give something like Novorapid as giving glucose. Short acting insulin because long acting may accumulate due to kidney disease. About 6-10 units. VOL? over 30minutes

Question 174

What will the glucose insulin infusion do that the calcium gluconate does not

Answer 174

Na/K ATPase pump Glucose to prevent hypoglycaemia Onset few mins, only lasts 4 hours

Question 175

affect of administering salbutamol in CKD and on insulin/ glucose? and very high K+

Answer 175

Activate NA/K pump, increase cellular uptake 😊 onset 20-30mins lasts about 4 hours.

Question 176

drugs that would increase removal of potassium from | body rather than just promoting uptake out of the extracellular compartment

Answer 176

Loop diuretic. Inhib co binding. LoH Addition fluids IV with loop diuretics. Water excretion through urine. At risk of hypovolaemia, may lead to AKI. If exchanging Potassium for Ca, may lead to hypercalcemia. GI adverse effects ? action over 24 hours. Removing K+ from body. Pros and cons.

Question 177

what other treatment should be considered if CKd patients serum K+ not improved? (too high atm)

Answer 177

Arrhythmias emergency dialysis.

Question 178

SGT: Ureteric colic and Urinary Incontinence whys metoclopramide prescribed? drug class?

Answer 178

dopamine receptor antagonist for vomiting

Question 179

If the kidney stone is in his ureter why did he feel the pain across his abdomen and down into his groin?

Answer 179

Kidneys and uterus share innervation. Referred pain

Question 180

How did the stone in ureter trigger such severe pain

Answer 180

Hyperperistalsis: increased jerky movement of smooth muscle= spasm or from stretch in mucosa. Inflammation or oedema. Increased pressure, prostaglandin release = vasodilation

Question 181

drugs thought to help stones pass through the ureter and reduce the need for surgery?

Answer 181

Alpha blockers: for patients with distal ureteric stones less than 10mm diameter. Also used for BP work by tightening muscles in walls of smaller arteries and veins so blood vessels remain open and relaxed. Improves blood flow, lowers BP. In ureteric stones: reduce ureteral spasm, increase pressure proximal to the stone, and relax the ureter in the region of and distal to the stone. Tamsulosin: pain triggered by hyperperistalsis. Relaxes smooth muscle that uterus made of. Increases fluid transport too= push stone down uterus Above 10mm: consider surgery. Below 5mm: drink water, wait for. Stone to pass Tamsulosin also used for blood presssure at end. Side effects: postural hypotension, dizziness, headache, dry mouth, cardiac palpitations, erectile dysfunction

Question 182

rationale for using hyoscine butylbromide? What are the potential adverse effects? in uteric colic

Answer 182

Anticholinergic: relaxes smooth muscle, inhibit uterus smooth muscle cholinergic. Possibly help? Constipation, risk of urine retention in elderly. May not be ideal

Question 183

interpreting the results of the two trials (sgt uteric colic case 1)

Answer 183

Randomised control trials: high up in hierarchy Doctor administering drug wasn’t blinded- possible confounding/bias. Lots of problems with this trial. No effective evidence. Systematic review would be best as looks at all them have one decision/value. Lack of evidence and all decisions should be informed by evidence.

Question 184

typical symptoms of urge incontinence, overactive bladder and stress incontinence

Answer 184

Urge incontinence/ Overactive bladder: sudden urge to urinate that’s difficult to control can be caused by cystitis, tumours, stones, obstructions. Overactive bladder: with/without urgency. Usually at night With incontinence: OOD wet and without: OOD? Dry Stress incontinence: involuntary leakage on effort or exertion, or on sneezing or coughing. NICE increase in abdominal pressure, urine leaks out

Question 185

how to determine type of urinary incontinence?

Answer 185

Detrusor muscle instability is it? | Dipstick test an look at b glucose, nitrite, lymphocytes etc in case it is a UTI or other infection.

Question 186

qs to ask about urinary incontinence?

Answer 186

* When does incontinence occur? Is it when sneezing, coughing/ on effort or exertion (likely stress urinary incontinence) * Is it sudden urgency and have frequency and nocturia (likely urgency incontinence UUI associated with overactive bladder syndrome) * Does incontinence occur without physical activity/ sense of urgency? May be other. * Voiding difficulty: straining, incomplete emptying sensation- may be chronic urinary retention (overflow incontinence) * Constant leakage of urine (may be intermittent if position dependent) — suggestive of a fistula (e.g. vesicovaginal).

Question 187

physiological and anatomical reasons for the development of stress incontinence?

Answer 187

Stress incontinence: Weakened pelvic floor from trauma to muscle- may be from birth: levator ani muscle, cant form tight sling Damage nerve supply to muscles and sphincters Detrusor relaxes with SNS, internal sphincters tighten through alpha adrenergic action to STORE URINE To VOID URINE: Detrusor contract PNS, internal sphincters relax. Before: bladder volume increases and M3 receptors allow stretch and stimulation so this can happen and urine can be released. Forceps/surgery delivery damage nerve supply.

Question 188

physiological and anatomical reasons for the development of urge incontinence?

Answer 188

• spontaneous detrusor muscle overactivty during bladder filling o Bladder pressure > urethral pressure = incontinence • Could be neurogenic: form stroke/ multiple sclerosis o Can combat with anti-cholinergic drugs block ACh neurotransmitter, usually treat asthma. Stop smooth muscle contractions • May be increased chance by caffeine and alcohol

Question 189

when to refer incontinence?

Answer 189

Urgent referral required for woman 45+ and unexplained visible haematuria (blood in urine) without UTI/ visible despite successful treatment of UTI. Or in women 60+ with same or dysuria/ raised white cell count. Suspected malignant mass from this area. Persistent urethral/bladder pain If associated with faecal incontinence: worry about 3rd or 4th degree tear= risk of infection Neurological diseases may cause Neurogenic all fistulae? Previous incotinence surgery: severe underlying damage perhaps

Question 190

investigations done in the community in women with incontinence?

Answer 190

Perform a general examination, • Examine the abdomen for a palpable bladder or a mass. • Perform a pelvic examination: • While performing the pelvic examination, also look for potential causes of urinary incontinence, e.g: • Evidence of pelvic organ prolapse. • Urethral diverticulum — a sac-like protrusion between the periurethral tissues and the anterior vaginal wall. • Pelvic mass. • Atrophic vaginitis.

Question 191

first line non-pharmacological interventions can help with urinary incontinence?

Answer 191

• Modify fluid intake • If BMI 30 or higher, lose weight • If have overactive bladder, trial reduced caffeine intake Reduce caffeine intake, pelvic floor exercises Ask to do bladder diary to help identify precipitating factors and monitoring effects of treatment. May not help urgency Monitor food intake. Be careful as still need to drink, don’t want AKI. Don’t drink too much. Approach with caution Min 8 pelvic floor muscle contractions min 3 times a day to try. Exclude/manage OBS. Parkinson’s MS, obesity, T2DM can increase urgency. ADRs may induce …. Diuretics- increase urinary frequency

Question 192

recommended first line drug treatments for overactive bladder?

Answer 192

antimuscarinic drugs, SNRIs and beta 3 agonists ``` Anticholinergics/muscarinics: • IR oxybutynin hydrochloride, should not be used in frail, older women at risk of sudden deterioration in their physical or mental health • tolterodine tartrate, • darifenacin ``` • The lowest dose should be used and titrated upwards if necessary. • Transdermal oxybutynin hydrochloride may be used in those unable to tolerate oral treatment. • Mirabegron may be used if treatment with an anticholinergic is contraindicated, ineffective, or not tolerated Treatment for minimum of 6 months See GP after 4 weeks- review treatment or sooner if any problems. If none, review again after 12 weeks then every 6 months (as over 75)

Question 193

examples of antimuscarinic drugs, SNRIs and beta 3 agonists | urinary- OAB

Answer 193

antimuscarinics (subtype of anticholinergics) - Oxybutynin. - Tolterodine. - Propiverine. ... - Darifenacin. ... SNRIs: (serotonin, Nad reup inhibi) - duloxetine - Savella (milnacipran) - Effexor (venlafaxine) beta 3 agonists: - Oxybutynin. - Darifenacin. - Muscarinic Antagonist.

Question 194

first line for urinary incontinence and SEs?

Answer 194

Anticholinergics constipation may be side effects/ indicate medicine is about to take effect Keep taking meds as may take 4 weeks to see results. May take longer for symptoms to improve. urinary retention

Question 195

SGT: IV fluids ``` Consequences of Over replacement (too much fluid) ```

Answer 195

* Fluid overload: pulmonary oedema, peripheral oedema * Impaired wound healing * Decreased tissue oxygenation * Electrolyte disturbances * Multi organ failure

Question 196

``` Consequences of Under replacement (not enough fluid) ```

Answer 196

* Reduced circulating blood volume * AKI-decreased renal perfusion * Hypoxaemia: low arterial blood oxygen level * Electrolyte disturbances * Multi organ failure

Question 197

whens IV fluid therapy given to patients?

Answer 197

to correct/prevent problems with fluid and/or electrolyte status

Question 198

Intravenous (IV) Fluids- The 5 R's | describe each

Answer 198

1. Resuscitation: fluid status assessed, hypovolaemic: req resuscitation urgently to restore circulation 2. Routine maintenance Patient cant meet fluid requirements orally/enterally e.g. Nil by mouth pre surgery and requires routine maintenance to meet normal daily fluid and electrolyte requirements 3. Replacement Fluids needed to correct water and/or electrolyte deficits/ ongoing abnormal losses such as high-output ileostomies, diarrhoea or vomiting which left untreated = hypovolemia/AKI/reduced organ perfusion 4. Redistribution severe fluid and elec disturbances, may be septic/critically ill/ following major surgery/ with major cardiac, liver or renal comorbities. Expert help required to manage IV fluid therapy in patient with complex redistribution needs 4. Reassessment fluid + biochemical status should be reassessed at regular intervals by health professionals as part of their monitoring of IV fluid therapy.

Question 199

``` IV fluids: normal values of.. Water Sodium Na Potassium K Chloride Cl- Glucose ```

Answer 199

Water 25-30mls/kg For elderly/frail, those with renal/ cardiac impairment or malnutrition 20-25ml/kg/day Sodium Na 1mmol/kg/day Potassium K 1mmol/kg/day Chloride Cl- 1mmol/kg/day Glucose 50-100g/day

Question 200

SGT IV Fluids consequences of administering this fluid regimen (too much water, Na, Cl , too little K+)

Answer 200

* Risk of oedema (peripheral and pulmonary) * Hypernatremia * Hypokalaemia * Hyperchloraemia ro * Acidaemia

Question 201

ongoing losses (IV fluid therapy)

Answer 201

``` vomiting+ nasogastric tube loss pure water loss (fever, dehydration, hyperventilation) biliary drainage loss diarrhoea pancreatic drain/fistula inapp urinary loss onngoing blood loss ileal loss jejunal loss ```

Question 202

IV fluid- why should K+ NOT be added to bags?

Answer 202

layering effect when added without asequate mixing. diff densities KCl prone to this serious effect on heart if pure K given !

Question 203

information should be looked at when assessing a patient’s fluid and electrolyte requirements?

Answer 203

ongoing losses... History of previous limited intake, thirst, quantity and composition of abnormal losses, comorbidities Clinical examination: -dehydration (Na, K, urea high or if had a billed/ been vomiting/ lying on floor and not eating/drinking), skin turgur (pinching skin) Colostomy /ilieostomy Respiration

Question 204

What clinical examination is important- IV fluids sgt

Answer 204

e.g. pulse, BP, JVP oedema, why would NEWS score, fluid balance charts, weight

Question 205

IV fluids- bags only come in what volumes, remember when making solutions

Answer 205

have 500ml or 1L bags= 1500ml or 2L.

Question 206

what may cause patient to have seizure from K falling TOO LOW?

Answer 206

Increased sodium chloride IV infusion= higher serum sodium levels and low Potassium. Hyponatraemic —> seizures . Dilution all hypokalaemia, Natraemia. Stop fluids completely and get expert to place the fluid- ITU specialist if NEWS score certain value.

Question 207

What other physiological problems can be caused by incorrect management of IV fluids?

Answer 207

Excess fluid = swelling, high blood pressure, heart problems, hypervolemia (excess water) in patients with CKD and renal failure as kidneys not removing excess fluid as they should. * Hypovolemia * Hypo/Hypernatremia * Peripheral/pulmonary oedema * Hypo/hyperkalaemia

Question 208

What are the five R's in IV fluids prescribing

Answer 208

Resuscitation, Routine maintenance, Replacement, Redistribution, Reassessment

Question 209

What is the amount of water needed for routine maintenance

Answer 209

25-30 mls/Kgs

Question 210

What is the amount of Na, Cl, K needed for routine maintenance

Answer 210

1 mmol/Kg/day

Question 211

SGT Immunology/Vaccination and Home Therapy What type of test is used to determine whether somebody has had chicken pox?

Answer 211

varicella serology

Question 212

What does a negative IgG and IgM antibody result indicate?

Answer 212

no previous exposure to varicella zoster virus nor immunity

Question 213

What does a negative IgG but positive IgM antibody result indicate?

Answer 213

no vaccination, current early stages of varicella zoster infection

Question 214

What does a positive IgG and IgM antibody result indicate?

Answer 214

previous exposure e.g. vaccination has failed, recent infection ..Have vaccine and disease

Question 215

What does a positive IgG but negative IgM antibody result indicate?

Answer 215

immunity to varicella zoster virus (vaccination), not infected

Question 216

what is XX used to indicate? a) IgG b) IgM

Answer 216

a) Previous infection/exposure. if + = antibodies made form vaccine perhaps b) infection recently if positive

Question 217

What vaccinations are currently available against varicella zoster virus in the United Kingdom.

Answer 217

``` 1. Chickenpox: • Varivax • Varilrix Shingles: • Zostavax- live attenuated varicella zoster virus vaccine Shingrix ```

Question 218

What diseases are caused by the varicella zoster virus

Answer 218

Chickenpox and herpes zoster (shingles) Latent virus lives in nerve cell bodies. After infection can reactivate in immunosuppressive or with age. Worried in pregnant women, children, immunosuppressed patients: weaker immune system, can be fatal- first infection

Question 218

What diseases are caused by the varicella zoster virus

Answer 218

Chickenpox and herpes zoster (shingles) Latent virus lives in nerve cell bodies. After infection can reactivate in immunosuppressive or with age. Worried in pregnant women, children, immunosuppressed patients: weaker immune system, can be fatal- first infection

Question 219

What are the risk factors for varicella infection- shingles?

Answer 219

- elderly - regular exposure to pre-school children - immunosuppression/comprised: neonate, pregnant, medication (methotrexate) - never been exposed to VZ virus via e.g. chickenpox so no antibodies - Comorbidities: R.Arthritis, Asthma, female

Question 220

name a med that causes immunosuppression

Answer 220

methotrexate

Question 221

What is VZIG?

Answer 221

varicella zoster immunoglobulin

Question 222

How is VZIG prepared?

Answer 222

from the plasma of donors who have a high titre of the antibody

Question 223

What are the indications of VZIG?

Answer 223

prophylaxis of those who: - are immunocompromised: pregnant, elderly, neonates, medication (prednisolone, methotrexate) - have been recently exposed to varicella zoster virus - have no antibodies to the virus

Question 224

Can VZIG be used in people already infected with chickenpox or herpes zoster virus?

Answer 224

no, | used for prophylaxis only

Question 225

How did the guidelines for treatment for VZIG treatment change post-2018?

Answer 225

shortage in VZIG means those qualifying for prophylaxis are now treated with acyclovir (antiviral) 3rd option oral/IV

Question 226

What are the symptoms of chickenpox?

Answer 226

- red itchy rash - fills with clear fluid, then ruptures - face, scalp, back

Question 227

What are the symptoms of shingles?

Answer 227

- itching, tingling, pain before rash appears - painful rash - affects ONE side of face/body

Question 228

Explain the relationship between shingles and chickenpox.

Answer 228

- chickenpox is first exposure to varicella zoster virus | - shingles is reactivation of virus in later stage

Question 229

What can lead to varicella zoster virus reactivation?

Answer 229

the immune system being compromised

Question 230

What age group does chickenpox affect most commonly?

Answer 230

children

Question 231

What age group does shingles affect most commonly?

Answer 231

adults (teens, young, elderly)

Question 232

whats anylosing spondylitis and affect on breathing?

Answer 232

inflammatory disease that, over time, can cause some of the bones in the spine (vertebrae) to fuse. This fusing makes the spine less flexible and can result in a hunched posture. If ribs are affected, it can be difficult to breathe deeply.

Question 233

describe the actions of TNF alpha and the rationale for blocking this cytokine

Answer 233

inflammatory, acute phase cyctokine produced by macrophages/monocytes in acute inflammation. causes: • endothelial activations • positive feedback on inflammatory cytokine cascades • systemic effects, apoptosis, fever, viral replication • cartilage destructins • bone erosion main thing: inflammatory response with IL6 and IL1 (other inflamm cytokines)role in acute and chronic inflammation. !!!

Question 234

whats TNF alpha critical in and what may happen if we block it?

Answer 234

critical in maintaining control over latent infection Would be blocked to prevent: Back pain, stiffness, fatigue, may be triggered by environmental factor in genetically predisposed individuals

Question 235

home anti-TNF alpha therapy - storage and disposal?

Answer 235

In a fridge (2°C-8°C) in its original container and protected from light until it's used. HUMIRA should never be put in the freezer or frozen. Can cause reactivation of latent TB- !!! Aggressive and widespread. TB screening before commencing TNF alpha. 14mg for this patient 12 weeks after treatment no response, check Aggressive and expensive medicine. sharps bin with needle.

Question 236

administering anti-TNF alpha

Answer 236

Injected every 1-4 weeks. Subcutaneous (in fat) May get rash at site of infection but treat more cautiously. Up to 14 days in up to 25 degrees avoid light Expensive Suppresses fever TB testing is expensive, van do skin test/ chest X-ray, interferon gamma release assays.

Question 237

Explain what pegylation is and why it is used with interferons

Answer 237

increases the amount of time the interferon remains in the body by increasing the size of the interferon molecule. PEG interferon: long acting. Interferons: cytokines with. Polyethene glycol

Question 238

immunological rationale for using PEG interferon in hepatitis C infection

Answer 238

enhance the immune response by stimulating the activity of immune cells and rendering virus-infected cells more susceptible to the responses of the immune system. Single stranded virus in liver. Flaviridie. Upregulates antigen presentation. Macrophages unregulated- engulf and destroy virus

Question 239

advice on the safe use and disposal of needles at home?

Answer 239

Put needles or similar medical supplies into the sharps bin immediately after using them and do not try to take them out again. Only fill the bin to where it says "Do not fill above this line". Keep your sharps bin in a safe place so it's not a risk to other people and is out of the sight and reach of children. Blood bourne transmission, put cap back on and dispose in sharps bin. Report all needlestick injuries

Question 240

side effects would you expect from interferon treatment

Answer 240

Side effects of alpha interferon in chronic hepatitis C: fever, headache fatigue, arthralgias, and myalgias are common, especially with the initial injections May be due to infection/ other drug side effects which would improve after first week. If no obvious infection try symptomatic treatment. … change dose. Haematological SE: anaemia, low white blood cells. Neutropenia, thrombo—Penia Counsel on any drug disorders.

Question 241

SGT Iron Deficiency Anaemia (microcytic) definitions of anaemia

Answer 241

Iron deficiency anaemia: diminished red blood cell production due to low iron stores in the body. Lower in pregnant women as increase in plasma volume, Generally lower in women than men as menstrual loss. Higher barrier/level of alert in men as no loss in menstruating.

Question 242

iron deficiency anaemia values

Answer 242

o Men over 15 years — Hb below 130 g/L. o Women over 15 years — Hb below 120 g/L. o Children 12–14 years — Hb below 120 g/L. Pregnant women — Hb below 110 g/L throughout

Question 243

features in the full blood count result would make you think that iron deficiency is the cause of a low haemoglobin concentration

Answer 243

serum ferritin level of less than 30 micrograms/L - but mau be hard to tell in infection/inflammation present as inc levels - less reliable in pregnancy * arrange a full blood count (FBC). * If results of the FBC show a low haemoglobin and low mean cell volume (MCV) check the ferritin level — check the ferritin level in all people with an MCV less than 95 femtolitres. Micro cystic: small cells. Hypochromia: low colour 30-35=normal Hb levels. 27 - low

Question 244

additional tests | to confirm iron deficiency

Answer 244

Ferritin: if suspect anaemia due to low iron. Micro cystic . • Below 15= unlikely to have other diagnostic. 15-100 Orr certainly 30-100. Hard to tell if iron deficient or not, may be other like RA… if over 100, can exclude. Vitamin B12 and folate levels

Question 245

Iron test results can be affected by: (3)

Answer 245

``` Medications o Antibiotics o Birth control pills and estrogens o Blood pressure drugs o Cholesterol drugs ``` Haemochromatosis: inherited iron overload condition Inflammation or malignancy = all tests difficult to interpret

Question 246

Why does iron deficiency cause anaemia

Answer 246

Iron is needed to form haemoglobin which form part of red blood cells that carry oxygen and remove CO2 form body. Iron is stored in Hb. Lack of iron means not enough blood to cells and tissues

Question 247

what problems can cause low iron levels

Answer 247

Iron is absorbed in jejunum duodenum in GI tract. Can be anything here that prevents absorption= deficiency. Absorption reduced through: • Coeliac disease • Some infections • Surgery: trauma from removing piece of gut. Gastroctemy

Question 248

Iron deficiency anaemia can be caused by:

Answer 248

• Heavy periods in women • Lack of iron in diet rare • Or loss greater than obtained. Likely here (menstruation) OR * Taking NSAIDs: cause gastric irritancies * Stomach ulcers * Bowel or oesophageal inflammation * Piles * Bowel/stomach cancers- less common carcinomas * Threshold: investigate ifanother cause i.e. cancer, better to pick up sooner. * Pregnancies: levels interpreted differently.

Question 249

how does iron enter body?

Answer 249

* Meat * Eggs * Dark green leafy veg * Fortified cereal and bread * Dried fruit * Pulses

Question 250

how does iron leave body?

Answer 250

* Blood * Sweat * Shedding intestinal cells

Question 251

iron storage in body

Answer 251

Iron stored in 2 states. Epi2+, ….. Iron deficiency. Can’t increase amount of iron reabsorbed. Vegetarians no necessarily iron deficient Don’t need a lot of iron, unless deficient than do to bring it up

Question 252

ferritin below what value - iron deficient... | and what range is hard to interpret?

Answer 252

below 15mcg/L as being iron deficient | range between 15 and 100mcg/L was difficult to interpret.

Question 253

what can can raise ferritin even in the presence of iron deficiency.?

Answer 253

inflammatory conditions

Question 254

how is iron lost from body (speed/ time)?

Answer 254

no route for iron excretion, rather a steady loss.

Question 255

additional tests/ considerations for loe Fe?

Answer 255

Cycles: frequent, heavy? Taking other meds? If no other obvious cause, get further investigated to exclude cancer etc. If it is menstrual, give iron supplement

Question 256

side effects with iron tablets (elemental not iron salt)

Answer 256

``` Adverse effects of iron supplements include: • Constipation. • Diarrhoea. • Epigastric pain. • Faecal impaction. • Gastrointestinal irritation. • Nausea. ```

Question 257

what are SEs with iron tablets linked to?

Answer 257

dose related and are directly related to the amount of iron absorbed (although the relationship between constipation or diarrhoea is less clear than for nausea and epigastric pain).

Question 258

when to take ferrous sulphate tabs?

Answer 258

works best on an empty stomach. Take it 30 minutes before eating, or 2 hours after eating. with orange juice or a vitamin C supplement. To lower pH, increase absorption Take with food or reduce side effects Antacids: raise pH of stomach, don’t take iron supplements with as absorption decreased Milk, tea, coffee can reduce too

Question 259

How much elemental iron should an iron deficient person receive per day? How many tablets of commonly available oral preparations does this equate to?

Answer 259

65 mg elemental iron (ferrous sulfate 200 mg) once daily (on an empty stomach) is needed to treat iron deficiency anaemia. One tablet a day NICE 2-3 times a day BNF

Question 260

which iron salts contain most elemtal iron in dose?

Answer 260

fumurate, sulphate

Question 261

how long it will take to replenish stores of iron?

Answer 261

2-3 months or a little longer

Question 262

symptoms of Fe overdose?

Answer 262

Acute nausea, vomiting, GI irritation. After oral ingestion, lasts up to 6 hours. Toxicity 6-24 hours: patient can go into remission, clinically stable but if taken large dose and nothings done, metabolic acidosis, convulsions, coma, liver damage, renal failure, pulmonary oedem, over 7 weeks, GI

Question 263

treatment of Fe overdose? MoA?

Answer 263

We can’t excrete the iron, treatment at A&E: desferrioxamine. Binds to free iron, makes complex which is then eliminated. ...iron chelator used for iron IV desferrioxamine mesilate given to chelate absorbed iron in excess of the expected iron binding capacity. In severe toxicity intravenous desferrioxamine mesilate should be given immediately without waiting for the result of the serum-iron measurement.

Question 264

whats desferrioxamine used for?

Answer 264

treating OD of iron (children) OD aluminium in dialysis patients • Transfusion regular for some bleeding disorders- become iron overloaded, cant excrete. Life of RBS = 120 days

Question 265

appearance of symptoms over time for iron overdose

Answer 265

1. Within the first 6 hours, direct toxicity to the gut may occur, without systemic toxicity. 2. 6 - 24 hrs symptoms may resolve, but there may be progressive absoprtion of iron, which may lead to hypotension, multi-system failure and coma. 3. This can result in hepatic damage between 12 and 96 hours, with bowel obstruction between 2-8 weeks. liver failure, jaundice, hypoglycaemia...

Question 266

sgt: macrocytic anaemia causes of macrocytic anaemia

Answer 266

Causes can be megaloblastic/ non-megaloblastic: - Vitamin B12 deficiency: oNutritional: strict vegan or oMalabsorption: gastric/ pernicious anaemia/ congenital lack or abnormality of intrinsic factor/ total or partial gastrectomy/ can be intestinal. oAutoimmune: Addisonian pernicious anaemia oGI: gastric/ terminal ileum problems (Crohn’s or TB) - Folate deficiency - Combined folate and B12 deficiency - Abnormalities of B12/ folate metabolism - Inherited defects of DNA synthesis/ methionine synthase

Question 267

absorption of vitamin B12 and its role in the production of erythrocytes

Answer 267

iron folate B12 in bone -> red cell mass -- > red cell destruction or Hb conc --> kidney binds to the protein in the foods we eat combines with protein IFso that it can be absorbed further down in the small intestine.

Question 268

problems associated with vitamin B12 deficiency

Answer 268

develop. .. anaemia, - HF as heart has to work harder other symtpoms of B12 def: • Vision problems • Memory loss • Pins and needles • Tingling in arms, legs- around sock area. ‘Hands and gloves’ as symmetrical, shortness of breath, rapid heart rate- palpitations • Non specific things- headache, loss of appetite, • Psychiatric conditions from mild to dementia • Diverse symptoms

Question 269

investigation and treatment of vitamin B12 deficiency

Answer 269

before starting folic acid, check... • allergic reaction to folic acid/any med • low vitamin B12 levels (vitamin B12 deficiency anaemia)/ pernicious anaemia + deficiency symptoms could be masked. Symptoms may be more disabling long term • Problem with this treatment: neulogical damage - nerves • have cancer (unless you also have folate deficiency anaemia) • on haemodialysis  • have a stent in your heart

Question 270

role of folate?

Answer 270

needed for maturing RBC and making DNA!! DNA synthesis !!

Question 271

what may cause LOW serum folate?

Answer 271

* Lack of dietary folate. Recommended daily intake is 200-250 micrograms * Nutritional: elderly, institutions, poverty, famine, diets, goats milk anaemia * Malabsorption: gluten-induced enteropathy * Excess utilisation: pregnancy, lactation, prematurity, haemolytic anaemias * Excess urinary folate loss: active liver disease, congestive heart failure * Drugs: anticonvulsants, sulfasalazine, antiepileptics, also drugs used to disrupt the folate pathway: methotrexate… * Liver disease, alcoholism, intensive care * Haematological malignancies. Haematological anaemia, C liver disease, -thyroidism

Question 272

what to question patient with low folate about?

Answer 272

* diet * Family history (of autoimmune disease) * Alcohol consumption * Folate in pregnancy * Cereals * Absorbed in upper part of SI * Body stores lasts for 4 months * Trimethoprim, Nitrofurantoin? * Inflammatory diseases

Question 273

folic acid treatment for low folate?

Answer 273

* 5mg daily for 4 months given * But if poor absorption, may take lifelong * Supplement in pregnancy where use if greater * Greens, brown rice, chickpeas, sprouts, asparagus, peas, broccoli. Sources of folic acid

Question 274

hows B12 absorbed in the body?

Answer 274

Absorption in body: • In stomach, B12 which is complexed to normal dietary proteins is released. • To prevent degradation, forms complex with haptocorrin for protection. • Gastric parietal cells also then release intrinsic factor, a protein produced in the stomach • Complex moves to duodenum (alkaline environment) if pancreas is normal functioning. • Intrinsic factor and complex arrive then new complex forms (from swap) • B12-IF complex remains stable until transported to terminal ileum. Last part of small bowel Vitamin B12 absorption in terminal ileum: • Cubilin receptor on luminal surface interacts with IF-Cbl complex and taken up into endosomes • IF and Cbl separated • IF degraded, Cbl attached to lysosomal transporter and sent to secretory vesicle. Forms complex with third protein: TC II. Transported uopt and distributed around body B12 deficiency leads to underdeveloped red blood cells that are larger than normal (megaloblastic anaemia).

Question 275

what does vit B12 (methylcobalamin) catalyse? ?

Answer 275

homocyteine -> methionine in DNA synethesis! need DNA to make erythrocytes. precursors

Question 276

less than how much cobalamin = B12 def?

Answer 276

Less than 200ng/L Cabalamin = B12 deficiency 97% of the time.

Question 277

Why do people develop vitamin B12 deficiency

Answer 277

• Pernicious anaemia: autoimmune condition of the stomach where cells that produce the IF are attacked so the body is unable to absorb B12. • Less IF produced, antibodies can attack parietal cells common cause of severe. OR • Antibodies specific for IF, less common, more age specific intestinal conditions- chrons disease

Question 278

Investigation for diagnosis: of B12 deficinecy? what about underlying cause

Answer 278

• Full blood count to determine MCV, haematocrit, Hb levels and blood film to identify megaloblastic anaemia • Measure serum cobalamin and folate levels Additional tests for underlying cause: • Liver function tests • Gamma-glutamyl transpeptidase • And or thyroid function tests Coeliac disease Gastric issues, surgeries gastrecomy Parasites

Question 279

qs to ask to investigate cause underlying - of B12 def?

Answer 279

* Tablets better if dietary input problem. Because if absorption problems, no point giving this way. * Can ask if vegan and taking PPIs?

Question 280

Why are hydroxocobalamin injections needed to treat deficiency in some people but not others

Answer 280

= form of vitamin B12. The injection form is more readily absorbed in the body and administered less often than oral tablets. Severe pernicious anaemia is usually treated with injections first.

Question 281

Damage to which parts of the bowel could cause vitamin B12 deficiency

Answer 281

digestive tract may be affected as lack of oxygen means less is reaching the gut so nausea and vomiting can be associated or diarrhoea. Crohns disease may cause it as long term inflammation of digestive system lining, body doesn’t get enough B12. May be absorption problems. Inflammation, had gastrecomy? Have to have IM injection. Bigger and painful but needed as cant take tablets.

Question 282

SGT: Anaemia of chronic renal disease causes of anaemia in chronic kidney disease

Answer 282

If your kidneys are damaged, they produce less of a hormone called erythropoietin which is needed to make red blood cells. This results in fewer cells being made and causes anaemia.

Question 283

management (investigation and treatment) of anaemia in chronic kidney disease

Answer 283

EPO therapy ... ..

Question 284

role of erythropoietin in the production of erythrocytes

Answer 284

hormone that is produced predominantly by specialised cells called interstitial cells in the kidney. Once it is made, it acts on red blood cells to protect them against destruction. At the same time it stimulates stem cells of the bone marrow to increase the production of red blood cells.

Question 285

normal pulse?

Answer 285

60-100bpm

Question 286

how would you decide if anaemia is due to chronic kidney disease

Answer 286

Determine iron status Below 60: start to investigate Above 60-likely another cause Hb to 110 or less Then check MCV: Marco/micro/normocytic anaemia determine which one. Renal patients normally nave normal anemia and low iron and folate- worthy checking levels ->Reduced erythropoietin in bone marrow. Other contributions: toxin build upo inn kidney- reduced half life of RBC- degrading Suspect anaemia: have long table of blood tests and serum ferritin or iron levels (but not alone- not enough). Need full picture

Question 287

target range of haemoglobin in CKD?

Answer 287

Male: 138 to 172 (g/L) Female 121 to 151 g/L.

Question 288

affect of severe anaemia in CKD patients?

Answer 288

Increase the chance of developing heart problems | • Arrythmias, extreme fatigue, increased cardiac output and cardiac death

Question 289

how to improve Hb levels- anaemia in CKD?

Answer 289

Erythropoietin therapy. Increase by 10-20g/L per month. Small incremental increase. Cardia and thrombotic events likely if increase all in one go. (Only for CKD patients)

Question 290

mechanism of action of erythropoetin.

Answer 290

directly interacts with EPO recpetor on RBC surface. triggers activation of several signal transduction pathways = proliferation and terminal differentiation of erythroid precursor cells, providing protection from RBC precursor apoptosis. Body (kidneys) make it naturallly. ?factor Works by stim bone marrow to make RBC. Erythroblastosis into reticulocytes (use nucleus) Then lose reticulum, results in RBC.

Question 291

cautions and contra-indications to starting erythropoietin therapy?

Answer 291

Cautious of hypertension. As EPO can increase uncontrollable. Ischaemic vascular. Disease too as can cause blood clots. Malignant disease- not used EPO in cancer/ chemo therapy unless anaemia symptoms present pure red cell aplasia : side effect of EPOs. - risk of Al tox - concurrent infection - thrombocytosis

Question 292

erythropoietin therapy | Monitoring?

Answer 292

blood pressure, reticulocyte counts, haemoglobin, and electrolytes—interrupt treatment if blood pressure uncontrolled.

Question 293

different types of erythropoetin available in the BNF

Answer 293

* EPOIETIN ALFA: tub side effect of pure red cell aphasia. * DARBEPOETIN ALFA: brand name?? * EPOETIN BETA * METHOXY POLYETHYLENE GLYCOL-EPOETIN BETA : brand name=??

Question 294

EPO/ EPO therapy end goal?

Answer 294

O2 delivery.= one term and acute physiological adaptations O2 used for a lot therapy:... Extend length of molecule to prolong half life= increases degree of response= have physiological effects for slightly longer. Administration: • IV: good for haemodialysis patients as will be in hospital anyway Don’t have to come in for it. • SC: slower absorption and longer half life. Easier to administer as patient can be trained. Depends on patient preference and cost as not enough evidence.

Question 295

Ferritin is usually higher in chronic diseases but lower in microcytic anameia- why?

Answer 295

higher in chronic diseases as it is produced as an acute phase reactant. However, it is usually lower in iron deficiency anaemia. Ferritin: acute phase protein, raised in infection. If they have infection, ferritin may be deceivingly high but patient may not be well.

Question 296

ideal ferritin levels?

Answer 296

Should receive to keep above 200 level. | But with non CKD: above 100mcg/L is fine for patients without CKD.

Question 297

how to prevent EPO induced hypertension (crisis) happening?

Answer 297

Monitor blood pressure before every dose!!! Would have seen an incremental increase and cause for alarm to review dose, bloods, Hb. Nurse administering should have been measuring/ he should have been counselled how and when to do this is administering himself. Also get INF/ bloods every month and no more than 10-20 increase of Hb every month. If higher increase, stop, reevaluate.

Question 298

benefits to using erythropoetin compared to a blood transfusion

Answer 298

Blood transfusion not recommended by NICE in these patients. Risks: develop antibodies against the new blood, viruses and infections may be introduces Pure red cell aphasia: reaction of EPO molecules – big risk of EPO. Related chronic iron overload- heart, lungs, liver affected= damage and failure. No mechanism for elimination of iron from body. May need iron chelation therapy if have overload. If epilepsy, get other teams teams involved, Blood disorder tea would also consider if patient is resistant to EPOs: RBC and reticulocytes may stop expressing EPO receptors and .

Question 299

sgt: drugs causing anaemia what drugs = deficite risk of haemolytic anaemia?

Answer 299

* Fluoroquinolones (including ciprofloxacin, moxifloxacin, norfloxacin, and ofloxacin) * Methylthioninium chloride * Niridazole [not on UK market] * Nitrofurantoin * Pamaquin [not on UK market] * Primaquine * Quinolones * Rasburicase * Sulfonamides (including co-trimoxazole)

Question 300

whats haemolytic anaemia?

Answer 300

(Reticulocytosis) increase in the rate of red cell destruction. RBC 120 days. Being destroyed faster than made here less than 20 days.

Question 301

What does the increased reticulocyte count indicate?

Answer 301

Reflects the bone marrows response to anaemia Reticulocytosis Trying to counteract [Being destroyed faster than made here] and produce more.

Question 302

Why is the mean cell volume increased in haemolytic anaemia/ reticulocytosis?

Answer 302

Reticolyctes are bigger than RBC. Usually due to folate/B12 deficiency but those normal and MCV only slightly increased.

Question 303

why may bilirubin and lactate dehydrogenase be increased? | haemolytic anaemia?

Answer 303

Hb breakdown increases bilirubin 3 types of jaundice. Haemolytic anaemia cause for prehepatic jaundice Lact- enzyme released. Usually keep inside cells. Sort of link to liver function tests lec. LDH end was looked at in cardiac damage not anymore. Not specific but both together good indicators of red cell damage.

Question 304

indicators of red cell damage? blood tests

Answer 304

bilirubin and lactate dehydrogenase increased

Question 305

Where does red cell destruction take place in haemolytic anaemia?

Answer 305

extravascular/ intravascular haemolysis (circulation) intravasc if can see sites on blood film - fragments broken down

Question 306

what does haptoglobin have a role in?

Answer 306

intravascular haem. Anaemia. Binds to free Hb as toxic to cells. Made by alpha ? In liver Level decreased as removed by Hb. Bound by it. – indicate intravascular together with fragments in blood film.

Question 307

mechanism for ciprofloxacin caused haemolytic anaemia

Answer 307

G6PD deficiency is a side effect of the drug, which can then cause haem. anameia

Question 308

whats GC6PD? (in haem anaemia)

Answer 308

GC6PD: without, don’t produce GSH which stabilises.. Reduces oxidative stress in cell More risk of having RBC damaged Inherited condition. Affects males, carried by females. X-linked recessive manner. = more risk of oxidation by these drugs. Female heterozygotes that carry this are more resistant to malaria. Therefore if you survive malaria, you’re more likely to pass it on. Would not prescribe any of the drugs in the list to patient with G6PD def.

Question 309

immune mediated mechanisms that can lead to drug induced haemolytic anaemia

Answer 309

``` AIHA Causes- When you have AIHA, your immune system makes antibodies that mistakenly attack your own red blood cells Drugs that can cause this type of hemolytic anemia include: Cephalosporins (a class of antibiotics), most common cause. ``` Ampicillin and high dose penicillins can cause. Or protein complex attached can lead to Methyldopa: unsure why happens. (It’s an old fashioned hypertensive- only often given in pregnant women as been used for so long and no adverse efffects)

Question 310

when does Lymphocytopenia/ lymphopenia occur? and causes what?

Answer 310

when your lymphocyte count in your bloodstream is lower than normal. Severe or chronic low counts can indicate a possible infection or other significant illness Cause for breathlessness- low Hb. Low Hb, reticulocytes: bone marrow not responding and making new cells.

Question 311

side effect of antimetabolite treatment?

Answer 311

Bone marrow suppression also: very low platelets so A shortage of blood platelets (thrombocytopenia) can lead to excess bruising, bleeding, frequent or severe nosebleeds, and bleeding gums.

Question 312

How might the azathioprine cause infection, fever, bruising?

Answer 312

Immunosuppressant, works by suppressing your immune system. This means your immune system becomes weaker. More susceptible to viruses etc. conversion Azathioprine -> 6MP (6 mercaptopurine) inhibits purine synthesis

Question 313

lack of TPMT enzyme leads to what?

Answer 313

Bone marrow suppression increased.

Question 314

what does TPMT do?

Answer 314

metabolises thiopurines into nontoxic, inactive products TMPT deficiency- get bigger effect from azathiprine as not converte to nontoxic and inactive. An still get reduced dose- consider how much its not working. Patients can be tested and depends if taking for IBS- gastro- probs wont test just tart on low dose. Rheumatology etc might test.

Question 315

important drug interactions that should be avoided in patients taking azathioprine

Answer 315

taking allopurinol !! Can increase risk of haemological toxicity. It’s a xanthine oxidase inhibitor. = get more 6MP going through. Same effect as not having TPMT. Used for high blood urine acid levels. Crystallises, inflamed joints (gout). * take ciclosporin or tacrolimus (immunosuppressant medicines) * take warfarin (used to prevent blood clots) * have recently had or are due to have any vaccinations (especially a "live" vaccine)

Question 316

affect of allopurinol (and DDI with azathiprine)

Answer 316

Allopurinol reduces active metabolite and vaccine ones are important • Can increase risk of haemological toxicity. It’s a xanthine oxidase inhibitor. = get more 6MP going through. Same effect as not having TPMT. • Used for high blood urine acid levels. Crystallises, inflamed joints (gout). Patient on azathioprine- don’t use allopurinol!

Question 317

monitoring is recommended for people taking azathioprine

Answer 317

Full blood count weekly. More frequently with high quality doses or if severe renal impairment. Monitoring for signs of myelosuppression Toxicity through treatment…. Monitor renal function- liver function tests

Question 318

SGT ADRs and DDIs | felodipine 10 mg od and swollen ankles link?

Answer 318

CCBs- lower BP work by preventing Ca entering cells of heart + arteries Ca causes heart + arteries to contract block Ca -> CCBs allow blood vessels to relax + open Peripheral oedema is a side effect of Felodipine as increased capillary pressure may lead to fluids leaking into surrounding tissues. Causes: renal/heart problems. To do with capillaries so diuretics wont help Side effect usually right after started drug

Question 319

interaction between grapefruit and calcium channels blockers.

Answer 319

=moderate increase in exposure to felodipine Reduce activity of cyp3a4 Opiates: metabolised by CYP2D6 Can cause irreversible inhibition of CYP3A4 (involved in many drug metabolism!!) Reducing presystemimc metab, hee: enzymes in inestinal wall Dose increase: explains why it happened after 12 months not yet. (look at timings in case)

Question 320

potential problems of starting amiodarone in patient on warfarin and has AF?

Answer 320

``` Antiarrythmic class III General side effects include: • Respiratory disorders • Nausea • Hyperthyroidism • Arrhythmias • Hepatic disorders ``` Severe DDI: Amiodarone and Warfarin (Vit K antagonist): Monitor INR

Question 321

mechanism of this interaction: amiodarone + warfarin?

Answer 321

Amiodarone: potent inhibitor of CYP450 enzymes responsible for warfarin metabolism. Decreased metabolism of warfarin = higher plasma concentrations and increased risk of bleeding complications etc. Inhibition of CYP2C9, 3A4,…