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Year 2 PBL > Unit 10: Diabetic Nephrogy > Flashcards

Unit 10: Diabetic Nephrogy Flashcards

1
Q

What is the role of hyperglycemia in activating the immune system and what are the consequences of this in diabetic nephropathy?

A

Hyperglycemia - production of reactive oxygen species and activation of pathways such as protein kinase C and AGE.
Causes inflammation - characterised by immune cells, cytokines and chemokines, including TGFbeta, VEGF - leads to inflammation fibrosis and increased vascular permeability.
Causes podocytopathy and intraglomerular hypertension resulting in proteinuria.
Increase in fibroblasts and chronic tubular injury as epithelial-mesenchymal celll transformation triggers in tubules.

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2
Q

What is the pathophysiology/ mechanism underpinning type 1 diabetes?

A

Is a combination of genetic and environment risk factors.
T cells react against beta cell antigens (breach of tolerance).
Brings about a cellular response against the antigen - resulting in the destruction of pancreatic beta cells due to autoimmune mechanism and inflammation - leading to a loss or reduction in insulin levels.

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3
Q

What are the consequences of low insulin in type 1 diabetes on the cellular level?

A

GLUT 4 is an insulin-dependent - transporter - is not inserted into cell membrane so cells cannot take up glucose from blood stream
lack of glucose in adipose tissue decreases fat synthesis and increases fat breakdown - FA are released into the blood and oxidised to ketone bodies
Hyperglycaemia leads to symptoms of diabetes.

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4
Q

What are the different antibodies in type 1 diabetes?

A

Anti-GAD (precurdor for glutamic acid required for GABA which causes release of insulin)

Anti- inslet cell antibodies

Anti-insulin antibodies

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5
Q

What are some of the genetic predispositions to type 1 diabetes?

A

Failure in maturation of T cells - results in escape of self reacting T cell - APECED
Mutation in HLA gene so better presents beta cell antigen to T cell (HLA-DQ and HLA-DR)

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6
Q

What are some hypothesised environmental triggers to type 1 diabetes?

A

Molecular mimicry - cross reactivity between forien antigen and beta cell antigen

Virus, toxin or repeated stress on the beta cells - results in crytpic antigen release - causing autoimmunity.

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7
Q

What are the key clinical presentations of T1DM?

A

Polyuria
Polydipsia (increased thirst)
Polyphagia
Weight Loss
Lethargic and Fatigue
Blurry visions
Nocturia
25% - Diabetic keotacidosis - vomittting and in severe cases coma.
Severe cases - altered mental status and deep and laboured breathing

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8
Q

What is the pathogenesis of type 2 diabetes mellitus?

A

Combination of genetic and life style risks - including obesity and inactivity
Increased levels of intraperitoneal visceral fat
Fat as an endocrine organ secretes Inflammatory markers, adipokines and free fatty acids
Complex mechanism can increase insulin resistance - beta cells respond to counteract this by increasing more insulin
Overtime, FFAs also inhibit GLUT2 on Beta cells so reduce glucose import, so unable to response to high blood glucose so reduced insulin secretion, become fatigued as insulin resistance increases - this leads to relative insulin deficiency and eventually absolute insulin deficiency - these patients present with hyperglycemia.
However, cant utilise blood glucose triggers physiological response observed in starvation - can cause diabetic ketoacidosis.

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9
Q

What are some risk factors for type 2 diabetes?

A

Age - older individuals beta cell mass declines so predisposed to insulin resistance as remaining beta cells become fatigued

Medications - corticosteroids, anti-psychotics and progestine only oral contraceptives

Obesity, lack of exercise, fatty diet

Genetic - high risk if first degree family relative

Gestational diabetes or given birth to a baby over 9 pounds

Are African American, hispanic or latina.

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10
Q

What are the common clinical presentations of type 2 diabetes?

A

Polyuria - nocturia
Fatigue
Polydipsia
Weight loss
Blurred vision
Ithciness around the genital area or regular bouts of thrush
Slow to heal cuts or ulcers

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11
Q

What are the microvascular complications of type 2 diabetes?

A

Retinopathy - blurred vision, risk of cataracts and glucoma, hyperglycemia causes damage to small blood vessels at the back of the eye - cause vision loss

Nephropathy - characterised by albuminuria across all stages, early GFR is elevated then progressively declines - riske of renal osteodystrophy, low calcium, high phosphate, high PTH, low VitD

Peripheral neuropathy - loss of sensation particularly in hands and feet, gangrenes and infected foot wounds due to damage to peripheral nerve and the supply blood vessels from hyperglycemia.

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12
Q

What are the macrovascular complications of type 2 diabetes?

A

Brain - increased risk of stroke, TIA and cognitive impairment
Heart - increase risk of coronary artery disease
Lower limb problems - peripheral vascular disease, narrowing of blood vessels - reduce blood flow to feet can result in slow healing feet wounds.

Main underlying factor - is causative of atherosclerosis due to hyperglycemia

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13
Q

Describe the micturition reflex when not urinating?

A

Not urinating - detrusor is relaxed (stimulated by sympathetic lumbar splanchnic nerve via hypogastric plexus and pelvic nerve NA at beta 3 receptors), internal urethral sphincter is contracted (sympathetic activation by NA alpha 1 receptors),
external urethera sphincter is contracted and the pelvic flood muscle maintain continence (stimulation of pudendal nerve S2,3,4)

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14
Q

Describe the micturition reflex when urinating

A

urination - bladder has filled, stretch receptors are activated and can relay to the spinal cord and brain. Activates the spinobulbospinal reflex
Parasympathetic pelvic nerve (ACh) causes contraction of the detrusor muscle, relaxation of the internal urethral sphincter parasympathetic, relaxation of the external urethra sphincter (pudendal nerve inhibition)
Parasympathetic - cause peristaltic contraction of smooth muscle in the urethra cause urination.
May be aided by valsalva manoeuvre to increase intrabdominal pressure.

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15
Q

What is meant by glycated haemoglobin?

A

Slow non-enzymatic covalent attachement of glucose to haemoglobin

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16
Q

What is the use of Hb1Ac blood test?

A

Uses levels of Glycated haemoglobin accepted as the international standard method for assessing glycemic control over the course of 3 months (or 120 days - is reflective of the life span of the rbc) and reflects.
Hyperglycemia causes Hb1Ac to increase - reflect previous three months, but one month before has the greatest effect on result
is directly proportional to ambient blood glucose concentration.

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17
Q

How to interpret HbA1C results?

A

A rise of 11mmol/mol in HbA1c is equivalent to a rise of 2mmol/L of blood glucose
Normal is below 42mmol/mol or 6%
Pre-diabetes is 42 to 47 or 6-6.4%
Diabetes is 48mmol/mol of over 6.5% or over

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18
Q

What factors can make Hb1Ac results inaccurate?

A

Factors that affect red blood cell lifespan
Low when low rbcs lifespan - sickle cell anemia, thalassemia
High when high rbcs life span - pernicous anemia, folate deficiency.

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19
Q

What is eGFR and how is it measured?

A

Is the flow of substance from blood from the glomerulus into the Bowman space over a specified period of time - rate of blood flow through the kidney.
Assessment of renal function
Estimated using renal markers such as creatinine (endogenous) CysC(endogenous) and inulin.
This is because we can predict the level that should be found in the blood and compare this to the level there actually is - hence determine the level of excretion from the kidney

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20
Q

What equations are commonly used when calcuating GFR?

A

Children: schwarts equation

Adults: Cockcroft-gualt equation
MDRD study equation
CKD_EPI equation

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21
Q

How does eGFR relate to the stage of kidney failure?

A

Stage 1 - Normal or high is above 90
Stage 2 - Mildly decreases 60-89
Stage 3a - 45-59ml/min
Stage 3b - 30 to 44
Stage 4 - 29-15
Stage 5 - below 15

Unit - ml/min

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22
Q

What is creatinine clearance?
How can it be used to estimate renal function?

A

The volume of blood plasma cleared of creatinine per unit of time

Used as value of renal function as can estimate the level of creatinine that should be present in the blood and urine - hence can compare to actual value.

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23
Q

What is the difference between creatinine clearance and eGFR?**

A

Creatinine clearance - creatinine specific - results can be skewed by other pathologies such as muscle damage - must be accounted for.

Creatinine clearance tend to be higher than eGFR particularly as eGFR declines.

GFR is preferred in clinical practice because it is easier to measure as creatinine clearance requires 24-hour urine collection.

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24
Q

What is the use of the albumin:Creatinine ratio to test for renal dysfunction?

A

Albumin is not normally found in the urine, creatinine is usually found in the urine.
If albumin is elevated indicates proteinuria - a sign of podocyte dysfunction indicative of damage to the filtration barrier
Hig value - indicates renal pathology - most often due to diabetes mellitus
Should be tested at diagnosis with DM and annually from then onwards

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25
Q

What is the risk of high cholesterol in diabetes?

A

Diabetic dyslipidemia
Inflammation and elevated levels of energy-rich substances - particularly lipids from lipolysis.
Results in increased hepatic and intestinal lipoprotein overproduction.
Increased small dense LDL and decreased HDL.
Hyperglycemia damage to endothelial cells makes it easier for plaque deposition to occur - increasing risk of cardiovascular complications such as stroke or atherosclerosis.

Also - linked risk factors of diet and obesity

26
Q

What is the effect of diet on cholesterol - negative effects?

A

Increased dietary cholesterol and fasting - decreases hepatic cholesterol production.

Dietary cholesterol is around 20-30% of total cholesterol.
High cholesterol can be caused by excessive dietary cholesterol intake
Main source in animal-derived fats - such as full-fat dairy products, animal fats, palm and coconut oil.
To lower LDL - avoid foods with saturated or trans fat (meat, chocolates, cheese)

27
Q

What are the effects of food on cholesterol - positive effects?

A

Foods to increase HDL - unsaturated fats - nuts, avocadoes, oatmeal, fish and soy.

Soluble fibre - binds and removes bile (including cholesterol) from body as part of waste - beans, avocados and lentils

28
Q

What are the effects of diet on HbA1C?

A

Decrease - low glycemic index foods as a source of carbohydrate including fruit, vegetables and wholegrain.

Increase - high glycemic foods such as sugary drinks, white bread, potatoes and white rice.

29
Q

How can diabetes cause damage to the kidneys?

A

Hemodynamic pathway - increased glucose in filtrate, increased activity of SGLT2, less Na+ delivery to macula densa - impairs tubuloglomerular feedback - leads to increased RAAS activation - resulting in constriction of efferent arteriole via angiotensin 2 - leads to increased GFR - hyperfiltration and increased pressure in the glomerulus can cause damage from sheer stress

Metabolic pathway - glucose bind with protein - form AGE - act directly or bind to RAGE - causes increased ECM deposition and increased mesangial cell proliferation - thickening of the basement membrane, loss of podocytes , increased permeability of the filtration barrier - decreased GFR

Hyperglycemia can also cause oxidative stress - release of DAMPs can cause an immune response triggering expression of growth factors and cytokines - further increasing the thickness and permeability of the basement membrane leading to diabetic nephropathy.

30
Q

What are the effects of hypertension on the kidneys?

A

Hyperfiltration in the glomerulus, damage from sheer pressure - release of DAMPs, attract inflammatory mediators, results in cytokine, chemokines and growth factor production - results in thickening of the basement membrane, increased ECM deposition and increased mesangial expansion - increased permeability of the barrier.

Systemic hypertension - thickening of stand narrowing the lumen of the renal artery and afferent arteriole - decreased renal blood flow - activation RAAS - exacerbated hypertension - increased damage to afferent arteriole and glomerulus.
Glomerulus sclerosis causes ischemic injury and eventually loss of the nephron. Decrease in GFR

31
Q

What is the ultrastructure in the glomerulus and how does it prevent protein loss?

A

Layer 1- endothelial cells - fenestratations allow the movement of soluble substances and fluid (not rbcs)

Layer 2 - basement membrane - is negatively charged so repels negative charged substances such as most proteins including albumin

Layer 3 - podocytes - attach to basement membrane via end feet, has narrow filtration slits between that vary from 25nm to 60nm in diameter - help prevent protein from being filtered into the bowmans capsule

32
Q

What is the cause of albumin in the urine?

A

Increased permeability of the filtration barrier
Often includes thickening of the basement membrane, widening of pores and podocyte damage.

Is always pathological

33
Q

What is the physical principle underlying haemodialysis?

A

Blood is removed and returned to the patient body by an AV anastomosis
When removed from body passes through a machine that contains a semi-permeable porous membrane (synthesis) that filters the blood.
Substances pass from the blood into the dialysate (which can be adjusted in content from pure water to contains certain salts and electrolytes etc)
1. Solutes move by facilliateated diffusion - gradient maintained by counter current flow of blood and dilaysate
2. Slightl pressure is applied to membrane and the difference in osmotic pressure causes water to move out of the blood by ultrafiltration
3. Large molecular weight substances and remaining soluts may then move by solvent drag/convection.

34
Q

How does renal dialysis operates in practice?

A

Typically offered to patients with a GFR below 15
Normally not recommended for patients who are extremely fragile
Can occur in hospital in a local dialysis unit or at home - depending on the type of dialysis chosen and the level of support thought necessary for the person.
Patient may be aided in their decision to have dialysis by a peer supporter, dialysis decision aid and a chronic kidney disease nurse.

35
Q

What are the advantages and disadvantages of haemodialysis?

A

+ treatment three days (normally only in 3/4 days for 4 hour treatment)
+ rapid correct of electrolytes

  • cause drop in blood pressure
  • risk of sepsis
  • AV anastamaosis may become thrombos, stenosis - making it unsuitable for use
  • diabetic patients arterial disease makes it difficult to gain sufficient access to blood supply
36
Q

What are the advantages and disadvantages of peritoneal dialysis?

A

+ every day and can be done overnight - easier to adapt to routine
+ slower correction of electrolytes so any side effects or potential electrolyte distubrance complication may be detected earlier
+ diabetic patients - does not require access to blood vessels so diabetic arterial disease is not a problem
+ better preservation of residual kidney function

  • risk of peritonitis, hernia and peritoneal sclerosis
  • requires high level patient engagement and understanding - usually only given to young motivated patients
37
Q

What is patient life expectancy like after the onset of dialysis?

A

Dialysis - accounts for 10% of kidney function
Kidney function still declines just at a slower rate
Average life expectancy of five to ten years
Varies: patients in 20s may gain 20yrs whilst patients above 75yrs or with additional health needs may only live an additional 2-3yrs.

38
Q

What is the cause of itchy skin in chronic kidney disease?

A

Medical term - CKD associated pruritus
1. Associated with build up of toxins in the blood stream which may irritate nerve endings.
2. Mast cells are activated which release histamin, histamine causes vasodilation and increase permeability of blood vessel wall, hence becomes leaky to substances which can then accumulate in surrounding tissues and damage cells
3. Reduction in the function of sweat glands due to dehydration and electrolyte imbalance in CKD patients.

39
Q

How does chronic kidney disease result in hyperkalemia?**

A

Decreased GFR
Decreased excretion of K+ in urine, eventually becomes less than the intake
Becomes more prevalent as CKD progresses, particular when GFR drops below 75% of normal

Also a risk factor os taking ACE inhibitors - reduced potassium secretion from the DCT.

40
Q

What are the consequences of hyperkalemia in CKD?**

A

Risk of cardiac arrhythmias and sudden death.
Muscle weakness
Vomiting.
Shortness of breath

Is a medical emergency

41
Q

How to manage to risks of hyperkalemia in CKD?

A

Monitor electrolyte levels whilst on ACE inhibitors, check within 1/2 weeks of initial dose, and 1-2 weeks after each increment increase in dose, monitor m ore frequently is abnormal results or increased risk.

Avoid food with high levels of potassium in them such as bananas, dried fruits, sweat potatoes and lentils.

In patients with diabetes - correct usage of insulin with cause the shift of K+ from the ECF to the ICF.

Ensure dialysis is of appropriate time length and dialysate components allow effective movement of K+ into the dialysate. (may need to reduce dialysate K+)

42
Q

What is the role of parathyroid hormone in regulating calcium and phosphate?

A

Parathyroid hormone
1. kidney - increase calcium retention and decrease phosphate retention.
2. Act on bone - indirectly stimulate osteoclasts to cause bone resorption - releasing calcium and phosphate into the blood
3. Activation of 1-alpha hydroxylase to produce calcitriol

43
Q

What is the role of FGF23 in regulating calcium and phosphate?

A

Produced in significant higher amounts in CKD - secreted by osteoblasts and osteocytes
Increases urinary phosphate excretion
Suppresses the production of calcitriol - leads to elevated PTH due to low calcium (due to lack of active vitamin D)

44
Q

What is the role of vitamin D in regulating calcium and phosphate?

A

Calcitriol produced in the kidney
1. Increase calcium retention in the kidney.
2. Activate bone resoprtion - to release calcium and phosphate into the blood
3. Increase absorption of calcium and phosphorus in the small intestine

45
Q

How does atorvastatin treat dyslipidaemia in type 2 diabetes?

A

Chemistry: is an anti-lempic, strucutral analogue to HMG CoA
Pharmacology - binds to HMG CoA reductase and inhibits it, prevents conversion of HMG CoA to mevalonate, therefore inhibits the production of cholesterol
Increases LDL receptors - leads to greater hepatic uptake of LDL so less in the bloodstream
Increases HDL production
Physiology: Reduced level of cholesterol in the serum plasma, increased proportion of HDL than LDL in the plasma leads to reduced risk of atherosclerosis
Clinical: used to reduce risk of atherosclerosis and cardiovascular complications resulting from elevated cholesterol levels.

46
Q

What is the mechanism of action of ramipril in CKD from diabetes?

A

Chemistry: Is an ACE inhibitor
Pharmacology: inhibits ACE, prevents the conversion of angiotensin 1 to angiotensin 2 - this inhibits the effects of RAAS
Also inhibits kininase 2 - leading to higher levels of bradykinin
Physiology: no vasoconstriction of bv, no production of ADH, no aldosterone production so no more sodium, no thirst response and water retention. This leads to a decrease in volume, which treats hypertension, which lowers the blood volume.
Bradykinin acts as a vasodilation. Prevents sheer damage to the glomerulus by decreasing blood pressure
Clinical: hypertension, symptomatic heart failure, prophalxais after MI, prevention of cardiovasculardisease, nephropathy.

  • relevant in early stage diabetic nephropathy to prevent temporary elevation in GFR
47
Q

What is the mechanism of action to dapagliflozin relevant to CKD?

A

Chemistry: is an SGLT2 inhibitor
Pharmacology: reduces reabsorption of glucose and sodium in the PCT, leads to increased glucose and sodium excretion in urine, this can help prevent hyperglycemia.
Increases sodium delivery to the macula activating tubuloglomerular feedback inhibits the activation of RAAS and increases the production of adenosine - leads to vasoconstriction of the afferent and prevents vasoconstriction of the efferent - leads to improved renal blood flow and decreased GFR and glomerular hypertension - this prevents damage to the glomerulus by sheer pressure.
Clinical indicating: hyperglycemia, early stage diabetic nephropathy, heart failure and hypertension

48
Q

What is the mechanism of action of metoformin?

A

Chemistry: anti-hyperglycemia, inhibits complex 1.
Pharmacology: targets hepatocyte cells taken up by OCT1 channel proteins - enters the mitochondria inhibits the electron transfer chain - leads to increased AMP: ATP ratio by inhibiting ATP production - high AMP leads to activation of AMPK.
AMPK phosphorylates transcription factors to increase the activity of enzymes in glycolysis such as hexokinase and insertion of GLUT4 into adipose and skeletal muscle.
Decreases activity of the enzyme in the gluconeogenic gene expression (particularly fructose-1,6-bisphosphate).
Leads to reduced blood glucose.

Also effects fat metabolism - reduces lipogenesis and increase lipolysis - cause weight loss.

49
Q

What is the mechanism of phosphate binders?

A

Chemistry: can be calcium or non-calcium containing
Pharmacology: bind to dietary phosphate hence are best taken with food, prevent the absorption of phosphate and encourage secretion in stool.
Physiology: to reduce phosphate levels in the blood, such as those seen in reduced kidney function
Clinical: hyperphosphatemia, CKD, end-stage renal failure, renal bone disease

50
Q

What is the mechanism of action of alpha calcidol?

A

Chemistry: non-endogenous vitamin D analogue, pro-drug as is inactive. Already contains a hydroxyl group at 1st carbon
Pharamcology: absorbed can bypass 1-alphahydroxylase as already has hydroxyl group at carbon 1, is acted on by liver by 25-hydorxylase to become active form of vitamin D calcitriol.
Physiology: increased calcium and phosphate absorption in the small intestine, increased renal retention of calcium, increased bone reabsorption to release calcium ions into the blood stream.
Clinical: patients with severe vitamin D deficiency or hpyocalcemia.

51
Q

What is the role of a CKD nurse?

A

Works in the MDT to provide high level support to patient and their families
Include inpatient and outpatient settings
Ensures appropriate patient education particularly around renal replacement therapy to ensure patient has informed consent and can make the best decision for them.
May undertake home visits
Assist transplant team with on-call transplant coordinator role.
Promote patient physical and psychosocial wellbeing
Monitor disease and treatment
Advocate and support for patients

52
Q

What is the role of a renal dietitian?

A

Support the patient to have good salt and water control, often recommend restricting dietary potassium, phosphate and protein.
Phosphate - meats, seafood
Potassium - bananas, lentils
Protein - animal meats, tofu, eggs

53
Q

How can diabetic patients be supported to follow a good diet?

A

Interaction with dietitian and chronic kidney disease nurse
NHS website - practical guidance, list of foods to avoid
Diabetes UK - recipe lists and instructions

54
Q

What are the different staff members that may be involved in delivering care to a diabetic patient in CKD?

A

Nephrologist - monitor GFR, renal replacement therapy etc
CKD nurse - patient support and advocacy
Dietitian - control blood glucose and diet to support rather than damage kidney function
Social workers - help individuals adjust to living with diabetes, deal with feelings, help reduce the psychological and social pressures on the patient, help with environment problems that may contribute to the disease (e.g organising support to travel to hospital)
Vascular surgeon - creating AV anastomosis for hemodialysis
Technicians - ensure dialysis machines are functioning correctly

55
Q

What is donor matching for a kidney transplant?

A
  1. Matching blood type (blood typing) - looking at ABO and rhesus
  2. Matching of HLA antigens - tissue typing - blood test to determine type of HLA antigens the recipient/donor has - (zero mismatch - means all the same), second blood test to determine antibodies produced against other HLA for the recipient only, is antibodies are found the recipient is considered HLA sensitive and should avoid a donor with these HLAs
  3. Serum Cross match test - blood of donor and recipient are mixed and observed for cross match (when recipient antibodies target donor blood), may be detecting by blood clotting or a fluorescent detection method.
56
Q

How can we measure quality of life?

A

AQoL-8D survey considers biological domains (3) and psychosocial domains (5)
Domains are:
Mental health, happiness, self-worth, coping, relationships, independent living, senses, pain.

57
Q

What is the link between depression and CKD?

A

1 in 4 patients with CKD will develop depression
More common in ethnic minorities, females and younger patients.
Disruption to life, decline in health - affect patient outlook on life, adapt feelings of hopelessness and worthlessness. Often combined with the loss of social connection
Predispose to depression
Often worsens health control leading to worse depression as more complications of ill-health.
Patients are often overwhelmed by life style changes and health demands

58
Q

How can depression increase risk of CKD?

A

Increased rates of obesity, sedentarism, immobility and alcohol use and smoking.

59
Q

What is the role of a CKD peer supporter?

A

Someone who is living through or has lived through the same illness/treatment as you.
Provide emotional comfort and information from the perspective of a patient on the biopsychosocial implications of illness and treatment.
trained to listen, maintain confidentiality and share what they know
May have face-to-face to one-to-one support sessions or online

60
Q

What are the pros and cons of a living donor?

A

+ increased success rate
+ higher availability (normally wait around 1 year)
+ surgery can be scheduled for a time that is best for the donor and recipient

  • more complicated ethical issues
61
Q

What are the pros and cons of a transplant of a cadaveric donor?

A

+ less ethical considerations around taking from the donor, as less risks

  • less effective, patient life expectancy reduced
  • longer waiting list, more likely to die before receiving a functional kidney.
  • surgery unplanned, drop everything and go, time pressure to ensure organ is still in usable condition.

Year 2 PBL (27 decks)

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