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KIDNEY (8) Flashcards

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1
Q
  1. What is the optimal pH of the body?
A

a. Around 7.4

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2
Q
  1. What happens if the body pH gets too far away from 7.4?
A

a. enzymes stop working and normal physiological process breakdown

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3
Q
  1. How can the body overcome the problem of getting too far away from the optimal pH?
A

a. The body has buffering system

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4
Q
  1. Howe can the body maintain buffering system and manage the products of that buffering?
A

that requires both the kidney and the lungs working properly

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5
Q
  1. Where is the kidney in the body and how does it look like?
A

a. Kidneys are paired structures that are located At the back of the peritoneal cavity

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6
Q
  1. How is the kidney supplied and how much does it take from the cardiac output?
A

a. Kidneys are being supplied by the renal arteries which receive blood from the aorta
b. It takes about 25% of the cardiac output

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7
Q
  1. What happens if the kidney becomes diseased?
A

a. Kidneys would have reduced blood flow and that leads to kidneys not working quite as well

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8
Q
  1. How much blood do the kidneys filter per/day?
A

a. 1500 L per/day

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9
Q
  1. How is the blood supply to the kidneys maintained
A

a. by reducing blood flow to other areas.

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10
Q
  1. What happens if someone is in shock?
A

a. they will get pail clammy extremities because their peripheral resistance is increasing to keep as much blood pressure as possible in your central vessels in your aorta and renal arteries
b. therefore, the kidneys carry on being perfused with blood that contains oxygen, nutrients (skin, peripheral muscles can go for few hours without having too much blood)

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11
Q
  1. list the functions of kidneys:
A

a. Filter 1500 L of blood per/day
b. Fluid balance
c. Acid-base balance
d. Na balance
e. Excretion including active excretion of toxins and some drugs
f. involved in endocrine control of:
i. Ca and bones metabolism
ii. Hb (haemoglobin)

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12
Q
  1. In which part of organ does blood filtration occur?
A

a. In glomerulus

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13
Q
  1. What is the working unit of the kidney?
A

a. Nephron

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14
Q
  1. Describe the blood filtration pathway:
A

a. Blood from aorta comes to the renal artery in the kidney.
b. Renal artery divides into smaller arterioles until it gets to the smallest arterioles that feed the blood vessels in the glomerulus.
c. Glomerulus filters small molecules and water where the blood keeps bigger molecules (e.g. proteins)
d. Large molecules remain in blood, pass into vasa recta.
e. Whereas, high volume of fluid leaving the glomerulus, going to the proximal convoluted tubule.
f. Then the liquid passes through the proximal convoluted tubule into the descending limb of Henle. Then back up to the ascending limb of Henle
g. From the ascending loop of Henle, the urine then goes to the distal convoluted tubule and then to the collecting duct
- Limb of Henle: perform as a countercurrent multiplier and that is where the osmatic gradient is generated that allows the volume of water and the concentration of salt in the urine to be decided and adjusted.

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15
Q
  1. Describe how Countercurrent multiplier works in the loop of Henle?
A

a. Descending loop is permeable to water and as we’ve got very dilute liquid in this tube therefore, water diffuses passively out of that
b. Fluid in LoH becomes more hypertonic.
c. Ascending LoH, wall permeable to Na and Cl but not water and as we’ve got concentrated fluid coming up the loop, sodium, and chloride can diffuse passively out down the concentration gradient into the blood.
d. Fluid becomes more concentrated.
e. Water and salt reabsorbed into the blood

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16
Q
  1. What is the function of the Loop of Henle?
A

a. Generate the osmatic gradient that allow the other processes go on

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17
Q
  1. What are the 4 groups of activities that we have in the kidney?
A

a. Passive reabsorption
b. Passive secretion
c. Active secretion
d. Active reabsorption

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18
Q
  1. Explain what passive reabsorption/ secretion is and give 1 example for each:
A
  • Passive reabsorption: is reabsorption passively down an osmotic gradient.
  • Example: the water in the descending LoH
  • Passive secretion – is secretion passively down a concentration gradient.
  • Example: NH4/ ammonium is passively secreted from cells into urine.
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19
Q
  1. How is ammonium secreted by the cells of LoH lining wall?
A

a. The cells of the lining of the LoH are metabolically active and they will produce metabolites including ammonium
b. Ammonium is secreted from the cells passively down the concentration gradient

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20
Q
  1. Explain what active reabsorption/ secretion is and give examples for each:
A

a. energy dependent process that actively pushes molecules either through the cell or out of the cell

Active secretion
* Drugs (penicillin)
* H+ and hydrogen ions

Active reabsorption
* Glucose
* Lactate

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21
Q
  1. Where does the final concentration of urine occur? And how is that process controlled
A

a. It occurs in the collecting duct
b. This process is controlled by Antidiuretic Hormone (ADH) which is secreted by the pituitary gland. In the pituitary gland the cells can sense blood pressure and blood osmolarity. The pituitary gland produces ADH when the blood pressure is Low and the osmolarity is high therefore, the ADH-dependent reabsorption in the collecting duct will stimulate reabsorption of water and that will lead to:
i. Increased water reabsorption
ii. Decreased urine output
iii. Increased blood volume which maintain the circulating blood volume

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22
Q
  1. Differentiate between diabetes mellitus and diabetes insipidus:
A
  • diabetes mellitus – sugar diabetes that is related to insulin, secretion of insulin, resistance to insulin, management of sugar levels in the blood. If this was untreated, or undiagnosed diabetes you get high thirst drive, and very high urine output
  • diabetes insipidus – In this case you get very a lot of very dilute urine that doesn’t necessarily contains any sugar in it. It is caused usually by tumors or injury to the pituitary and that means the patient cannot secret ADH and therefore, ADH-dependent water reabsorption in the collecting duct doesn’t happen resulting in up passing a lot of very dilute urine as the body cannot concentrate its urine
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23
Q
  1. what is Renin-Angiotensin System? And how does it work?
A

a. This is group of cells that is called Juxta-glomerular apparatus (JGA).
b. It is a point of contact of glomerulus and distal tubule/collecting duct.
c. The cells there can senses reduction in blood pressure, urine concentration.
d. If they sense drop in the Bp or increase in the urine concentration, then they will release Renin hormone

e. Renin catalyses conversion of angiotensinogen (from liver) to angiotensin 1
f. ACE catalyses conversion of angiotensin 1 to angiotensin 2. Leads to vasoconstriction increased BP
g. angiotensin 2 act on the adrenal gland and stimulates the secretion of the aldosterone  increased water and Na retention.
h. Therefore, produce concentrated urine  maintain BP

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24
Q
  1. What are the Signs/symptoms of kidney dysfunction
A
  • change in urine output
  • Dark urine
  • Proteinuria
  • Haematuria
  • Na/K imbalance
  • Fluid retention
    o Oedema
    o Hypertension
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25
25. What problems might arise if you had Proteinuria due to kidney dysfunction?
a. Losing proteins --> can interfere with your metabolic status --> could have problems with e.g., healing, weight-loss b. Losing proteins --> also can interfere with the balance of extracellular and intracellular fluid
26
26. Why could people with kidney dysfunction have oedema?
a. Due to fluid retention so, people could might have Low urine volume  fluid retention  fluids tend to set where gravity puts it (tends to pool closes to the floor)  Oedema in your ankles (puffy Oedema)
27
27. What is pitting oedema? And what does it associate with?
a. is where you press on the tissues for few seconds and take your thumb away, the indentation of your thumb will stay there which is a sign for fluid retention). b. Usually associated with heart failure, but also can be associated with kidney failure
28
28. What could be a consequence of problems with fluid balance/ fluid retention?
a. hypertension
29
29. what could patient get in Acute Kidney Injury?
a. Decrease in urine output b. Decrease in secretory function c. Impaired Na/K balance
30
30. What can cause AKI?
There are many causes including: a. Pre-renal: dehydration,  Low blood pressure  low fluid volume  heart not pumping very well  cannot maintain pressure in the kidneys  kidneys are going to be perfused  acute kidney disease  low BP, heart failure, myocardial event or lost lots of blood due to trauma b. Intra-renal:  inflammation, embolism, scarring/damage to nephron  inflammation: Lots of inflammatory products in the blood  these products going to be clubbed in the filter/ or you get complement deposit in the filter  Embolism: if you get clot. If it goes down into the aorta or into the renal artery, it can then embolise in your kidney and stop that kidney being perfused). These can cause scaring and damaging to the nephron c. Post-renal: obstruction, stones  If the flow of urine from the kidney into the ureters is blocked by stones or cancer or scaring from previous surgery etc..  obstruction of that  whatever gets there dammed up in the kidney  kidney filter will not be able to work and stop working
31
31. Is there any group of people who are at higher risk?
a. Elderly people and people who has got pre-existing heart disease/ kidney disease, people who had trauma, or collapsed --> kidney has got less reserve --> more problem
32
32. How could infective endocarditis lead to AKI?
a. People can get embolism of clots from the vegetations that go out into the circulation. If it goes down into the aorta or into the renal artery, it can then embolise in your kidney and stop that kidney being perfused leading to AKI
33
33. What happen if the embolism in infective endocarditis went upward or downwards?
a. If it went upwards, it could cause stroke b. If it went downwards into the lungs it can lead to pulmonary embolism
34
34. How to manage AKI?
a. To have low threshold for suspicion and to get their doctor to check b. If the patient was pre-existing chronic kidney disease, elderly, heart disease that means they are at more risk of developing AKI c. Unwell, trauma, dehydration are at more risk of developing AKI
35
35. How to treat AKI?
a. Refer early: may require hospital admission b. Assess urine output (>0.5ml/kg/hr) c. Blood tests: urea, creatinine, Na, K. d. Manage fluid balance carefully – measure how much urine has been produced + replacing that volume of liquid so that the patient doesn’t get further dehydrated (not overloading just fluid replacement) e. Manage Na/K balance carefully f. Careful selection of drugs – many drugs make kidney injury worse (avoid them)
36
36. What cause or lead to chronic kidney disease?
a. May follow AKI b. CKD more associated with more as Atherosclerosis, Hypertension, Diabetes c. SLE d. Scleroderma e. Renal stones
37
37. What is the link between diabetes and CKD?
a. Diabetes has both macrovascular and microvascular complications. One of the microvascular complications of diabetes along with retinopathy and peripheral neuropathy is nephropathy which can lead to CKD
38
38. What is the link between SLE and CKD?
a. Systemic lupus erythematosus is connective tissue disease characterized by wide-spread inflammation and inflammation can impact on the kidney causing chronic kidney disease
39
39. How could renal stones lead to CKD?
a. It causes post renal AKI and if that isn’t managed then you can develop chronic kidney disease
40
40. Chronic kidney disease tends to present with:
a. Hypertension b. Na retention c. Because you have got hypertension, you might have fluid overload, you can get Heart failure o Hypertension  fluid overload  heart failure d. CKD could impact on drug metabolism o Avoid NSAIDS
41
41. How to investigate CKD?
a. BP b. Urinalysis – check for: i. Protein, glucose, blood c. Blood tests i. FBC – full blood count (there is relevance between FBC and anemia to kidney disease) ii. Urea, creatinine, Na, K d. Imaging i. Ultrasound ii. CT/MRI
42
42. What test could we use to check if there is blood or protein in the urine?
a. Dip stick
43
43. How to manage CKD?
a. Manage underlying causes b. Manage BP c. Manage Na/K balance d. Manage fluid balance
44
44. What is the first step of stepwise processes in managing CKD?
a. Renal dialysis
45
45. What does renal dialysis mean?
a. Taking the blood out and do what the glomerulus cannot do for us because of the kidney disease i. Filtering the blood  adjusting the fluid levels + adjusting salt levels  put it back in
46
46. What are the 2 common types of renal dialysis?
a. Haemodialysis b. peritoneal dialysis
47
47. What is Haemodialysis?
a. Producing an arteriovenous fistula i. arteriovenous fistula is produced: short cup between an artery in the arm and vein in the arm and produce a short circuit ii. take the blood from the artery --> filter it --> put it back in the vein
48
48. What is peritoneal dialysis
a. peritoneal cavity: big cavity in the abdomen i. Big cavity  big surface area we can exchange fluids and exchange salt across it b. Flood the peritoneal cavity with fluid and overtime because of osmotic gradient you get passive exchange of water and salt across the peritoneal membrane out of the blood and into the blood and out of that fluid and into that fluid and then you can drain the fluid off
49
49. How many times people with kidney disease can make dialysis?
a. 2 or 3 times a week
50
50. What can we do in case of failure of the 2 forms of dialysis? Or in case the patient wants another treatment option?
a. Renal transplant
51
51. Do we need to put the transplanted kidney in the same place of the original kidney? Justify your answer. How will it work?
a. No, that is difficult to access, we Just need to put the new kidney above the hip, into your pelvis and your lower abdomen. b. The artery, the vein, and the ureter can be connected so, it carries on producing urine
52
52. What are the requirements for a kidney transplant?
a. we need tissue typing b. kidney donors: live or dead i. if dead must be suddenly or left-brain dead-on ventilator intensive care c. immune suppressants
53
53. Why do we need tissue typing in transplants surgeries?
a. Due to the risk of rejection as there is high chance that patient is going to reject that e.g., kidney. because your immune system would recognize it as foreign b. this is due to the major histocompatibility complex
54
54. what is major histocompatibility complex?
a. Is the complex of antigens that are responsible for recognizing self and non-self
55
55. What risks could using immune suppressants by people who had transplants lead to?
a. Immune suppressants put patients at risk of developing: i. Infection ii. Cancer
56
56. How could using immune suppressants lead to cancer?
a. because the immune system doesn’t just only deal with infection but, also recognizes cancer cells and kill off them
57
57. why do people who had transplants need to be followed up regularly?
a. To check if their transplants get rejected b. To check things regard their cancer risk
58
58. What complications CKD might have?
a. Anaemia b. Bleeding c. Complications with calcium and bone metabolism
59
How could CKD lead to Anaemia
a. Erythropoeitin (EPO): hormone that is produced by kidney b. EPO Stimulates proliferation of pluripotent stem cells in bone marrow, maturation of RBCs. c. Reduced production of EPO because of kidney disease d. CKD may lead to anaemia (because of the hormone deficiency)
60
60. How could CKD increase the bleeding risk?
Bleeding is multifactorial but in CKD; a. They have abnormal platelet formation b. Abnormal platelet/vessel wall interaction (Virchow’s triad) i. abnormal binding between the platelets and the vessel wall interaction c. Patient who are undertaking dialysis would be anticoagulated d. Therefore, slightly increased risk of bleeding following extractions/surgery
61
61. How to manage bleeding in CKD patients after tooth extraction?
a. Bleeding in this group of people is not to the point where we want to avoid it. b. but, we need to be aware of, so warn the patient and manage them with local measures
62
62. What does Virchow’s triad consist of?
a. vessel wall b. blood flow c. clotting factors
63
63. how could CKD interfere with calcium and bone metabolism?
a. Vit D3 required for Ca absorption in the gut and bone formation. b. Vit D3 produced in skin and liver, from diet i. Vitamin D produced in the skin from the UV sunlight and in the liver from the diet. But, this is not. The active form c. Converted to active form (1,25 dihydroxyvitaminD3) in kidney. i. Vitamin D is converted from inactive for to active form in the kidney d. CKD leads to reduced levels of active D3 e. Loss of negative feedback leads to increased Parathormone i. The parathormone hormone secretion is increased by the parathyroid gland ii. Parathormone function: mobilises osteoclasts and it is normally secreted in response to low calcium levels. It sets off and binds to your osteoclasts and tells your osteoclasts to start mobilising bone because we want as much calcium s we can get iii. Kidney disease --> increased levels of parathormone --> increased bone turnover --> renal osteodystrophy and they can also develop giant cell lesions iv. Patient can develop renal osteodystrophy f. PTH causes stimulation of osteoclasts g. Increased bone turnover. h. Giant cell lesions of bone (often present in maxilla and mandible) i. Giant cell lesions: Clumps of osteoclasts and other giant cells. You can get this in any bone but, it is very common in the jaw. Can present like cyst or like little tumors and they are hormone driven
64
64. What are the group of drugs that act on the kidney?
a. Diuretics i. Thiazide ii. Loop diuretics iii. K-sparing diuretics iv. Osmotic diuretics b. ADH/vasopressin
65
65. What are Diuretics taken for?
a. they are not taken for kidney disease but, people tend to take them for heart failure and for heart disease
66
66. give a brief of Thiazide diuretics (Bendroflumethiazide).
a. Used in heart failure, high BP. b. Inhibit Na resorption in distal tubule c. Reduced osmotic gradient i. Because you have got less Na resorption in the distal tubule you cannot develop full osmotic gradient. Therefore, kidney is less able to resorb water d. Less passive resorption of water e. Increased urine volume i. Diuresis means producing a lot of urine f. the problem is that thiazide also interfere with countertransport of K: i. Increased countertransport of K g. Thiazides are actively secreted and compete with other organic acids eg uric acid: may precipitated gout i. If you have goat or pre-dispose to gout and you take Thiazides, they are actively secreted in competition with other organic acids. That means if you are secreting you Thiazides for your kidney you cannot secrete your uric acid molecules in your urine and your blood uric acid will go up
67
67. What does Increased countertransport of K result in?
a. Hypokalaemia which is low blood potassium levels
68
68. Is Hypokalaemia problematic?
a. most of the time isn’t a problem but, sometimes can be a problem especially If you have got pre-existing heat disease such as atriofibrilation
69
69. give a brief of Loop diuretics
a. Used in heart failure, high BP. b. Inhibit Na/K reabsorption in thick ascending LoH i. May cause hyponatraemia – low Na levels ii. May cause hypokalaemia – low K levels
70
70. What are the 2 groups of diuretics that can cause problems with K? what should patients do in this case?
a. Loop diuretics and Thiazide b. patient may need to take K supplements
71
71. Give a brief of K sparing diuretics.
a. Inhibit aldosterone dependent Na reabsorption in distal nephron. b. Reduced negative potential in lumen causes decreased secretion of K. c. Increase serum K levels therefore, we don’t need to take K supplements
72
72. Give a brief of Osmotic diuretics
a. Large molecules b. Filtered in glomerulus c. Too large to be reabsorbed therefore, they stay in the LoH and in the collecting duct. so, they cannot be brought back to the blood and they cause osmotic potential in the lumen d. Osmotic potential in lumen leads to reduced water reabsorption
73
73. What type of diuretics would you use for patients who are having long operation? And why?
a. we need a very quick diuretics for the patient. b. You might use mannitol drug that is osmotic diuretic to produce diaeresis. c. Neurosurgeons also, need to control urine volume very carefully and they might use mannitol to manage fluid balance levels for patients who had head injuries
74
74. Why do we need to be careful with drug prescriptions with people with kidney disease?
a. We need to think how these drugs are being metabolized b. Is there any risk making AKD worse?
75
75. What else in addition to kidney disease management, do you need to do with patients with other systemic disease?
a. Diabetics, smokers, patients with hypertension, patients with heart disease or atherosclerosis are at risk of kidney disease --> you need to give them message to maintain their QoL and their survival. Then manage those predisposing factors and other disease that predispose to kidney disease

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