Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Med Yr2 > Urinary and thirst > Flashcards

Urinary and thirst Flashcards

1
Q

Diabetes complications - acute: (3)

A
  • Diabetes ketoacidosis: DKA (usually T1D)
  • Hyperglycaemic hyperosmolar state: HHS (usually T2D)
  • Hypoglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DKA characteristics (usually T1D)
- Glucose
- osmolality
- Ketones
- pH
- Hydration

A
  • glucose > 11mmol/L
  • Variable osmolality
  • Ketonaemia >3mmol/L
  • Acidosis pH < 7.3
  • Less severe hypovolaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HHS characteristics (usually T2D):
- Glucose
- osmolality
- Ketones
- pH
- Hydration

A
  • Marked hyperglycaemia (>30mmol/L)
  • Marked serum hyper osmolality (320>Osm/kg)
  • <3 mmol/L
  • no ketone driven acidosis
  • Hypovolaemia (severe dehydration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diabetes complications - chronic: microvascular (3)

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diabetes complications - Macrovascular: (3)
- C A
- C
- P

A
  • Coronary artery disease
  • Cerebrovascular disease
  • Peripheral vascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Poloyol pathway: (damage)
- Produces reactive….
- which cause damage to ….

A
  • Produces reactive oxygen species which cause damage to blood vessels and endothelium, may cause neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Protein kinase C pathway:

A
  • Causes a variety of issues
  • Activation increases VEGF causing new vessel formation in the back of the eye. These new vessels are ineffective, causing retinopathy and retinal bleeds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mechanisms of action for oral agents of DM
- Metformin
- Sulfonylurea

A
  • Metformin: suppression of hepatic glucose
  • Sulfonylurea: Increase in insulin secretion from beta cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mechanisms of action for oral agents of DM:
- GLP-1 Agonist
- DDP-4 inhibitors
They’re linked

A
  • DPP-4 inhibitors – inhibit GLP-1 degradation,
  • GLP-1 agonist – promotes glucose dependent insulin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sites of haematuria:
1. Glomerular
2. Non-glomerular (4)

A
  1. Glomerular
    - Glomerulus
  2. Non-glomerulus
    - Kidney
    - Ureter
    - Bladder
    - Urethra
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Flexible cytoscopy:

A
  • A flexible cystoscopy is a test that allows the doctor to look directly at the lining of the bladder, from the opening of the urethra. During the procedure a thin flexible ‘fibre-optic’ tube called a cystoscope is passed through the urethra
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CT urogram:

A
  • used to examine the kidneys, ureters and bladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sensitivity of visible haematuria for detecting cancer:

A
  • Positive predictive value of haematuria for detecting cancer, especially in men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Risk factors for kidney or urinary tract cancer: (4)

A
  • Age
  • Smoking
  • Exposures to benzene, aromatic amines (dyes, road fumes), carcinogens, chemotherapy, high doses of analgesics
  • History of: Irritative voiding symptoms, Chronic urinary infections indwelling urinary catheter, pelvic irradiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Glomerular causes of haematuria: (3)
- Antibody caused
- AN…
- Thin ….

A
  • IgA nephropathy (+/- HSP)
  • ANCA vasculitis
  • Thin nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Non-glomerular causes of haematuria: kidney (3)

A
  • Cancer
  • Stones
  • Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Non-glomerular causes of haematuria: Ureters (2)

A
  • Cancer
  • Stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Non-glomerular causes of haematuria: bladder (4)

A
  • Cancer
  • Infection
  • Non-infective cystitis
  • Stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Non-glomerular causes of haematuria: Urethra (3)

A
  • Cancer (prostate)
  • Infection (prostatitis)
  • Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical approach to haematuria:
- Confirm
- Check
- When
- Check

A
  • Confirm haematuria by using a dip stick
  • Check history for specific cause
  • When appropriate, screening of whole urinary tract for cancers
  • Check glomerular causes, rarer but still a possibility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Raised hydrostatic capillary pressure origin example : rise in venous pressure (3)

A
  • Left heart failure: pressures rise in the dependent (pulmonary) circulation
  • Insert pulmonary catheter to find pulmonary capillary pressure
  • If PCP rises above 25mmHg then frank pulmonary oedema occurs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Systemic oedema:
- How
- Where

A
  • Results from raised pressures in the systemic venous circulation leading to fluid accumulation in the interstitial spaces
  • Often affects the lower body; legs, feet and ankles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Pitting oedema:
- Causes (2)

A
  • A result of either a systemic problem, (heart, kidneys, liver function)
  • Or localised problems with veins in the affected area (pregnancy and deep vein thrombosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Increased extravascular colloid osmotic pressure due to an increase in π i
- What causes it
- How
- When

A
  • Capillary leak syndrome
  • The release of cytokines causes proteins to accumulate in the extravascular space
  • Occurs in sepsis and burns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Interstitial fluid: transudate
- Filtrate of…..
- Protein content
- Caused by (2)

A
  • A plasma filtrate
  • low protein content (<30 g/l
  • increase capillary hydrostatic pressure i.e. cardiac/nephrotic/renal failure
  • Reduce colloid osmotic pressure i.e. malnutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Interstitial fluid: exudate
- Filtrate of…..
- Protein content
- Caused by, example

A
  • plasma
  • High protein content: >30 g/l
  • Factors that increase extravascular colloid osmotic pressure, i.e. increased capillary permeability to protein (burns, sepsis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Capillary hydrostatic pressures (P):
- Generated by ….
- What does it cause?

A
  • Propulsive forces
  • When Pc > Pi , net filtration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Colloidal osmotic pressures (π):
- Generated by ….
- What does it cause

A
  • Impermeable protein concentrations
  • when πc > πi , Net absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Reduced plasma colloid osmotic pressure (πc): Nephrotic syndrome - explanation
- Presentation

A
  • Nephrotic syndrome: damage to basement membrane of the glomerulus results in proteinuria and hypoalbuminaemia
  • Oedema around the eyes, puffy face, pitting oedema of feet and ankles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Reduced plasma colloid osmotic pressure (πc): impaired protein synthesis
- Causes (3)
M
M S
I H S

A
  • Malnutrition: reduced protein intake causes oedema around the belly (Kwashiorkor)
  • Malabsorption syndromes: Pancreatic insufficiency, Cystic fibrosis, Intestine surface damage
  • Impaired hepatic synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Common causes of transudate effusion (increase in Pc or decreased π): (5)
- C/H/R
- N S
- P D
- P
- P E

A
  • Cardiac/hepatic/renal failure
  • Nephrotic syndrome
  • Peritoneal dialysis
  • Pericarditis
  • Pulmonary embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Common causes of exudate effusions:
- P/TB
- I C
- C
- P
- P E

A
  • Pneumonia/TB
  • Inflammatory conditions
  • Cancer
  • Pancreatitis
  • Pulmonary embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Non-cardiogenic pulmonary oedema:
- What is it?
- What causes it?

A
  • Pulmonary oedema with no increase in pulmonary wedge pressures >18 mmHg
  • Results from increased permeability of pulmonary capillaries from a direct or indirect pathological insult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Acute Respiratory Distress Syndrome (ARDS): causes
- F O
- P
- I I / D
- Re-E
- N C
- H A E

A
  • Fluid overload
  • Pancreatitis
  • Inhalation injury / drowning
  • Re-expansion of lungs after draining
  • Neurogenic causes - head trauma / haemorrhage
  • High altitude exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Acute Respiratory Distress Syndrome (ARDS):
- Definiton (specific to…)
- Diagnosis requires (3)

A
  • A non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome (SPECIFIC)
  1. Acute onset (1 week)
  2. Bilateral opacities on chest X-ray
  3. PaO2/FiO2 ratio of <300 on PEEP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Ascites:
- What is it?
- What causes it?

A
  • Fluid accumulation in the abdomen
  • Portal hypertension, due to cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Ascites: portal venous pressure increase causes (4):
- H D & F
- R P-H V P
- R H V D
- I V F

A
  • Hepatic damage and fibrosis
  • Raised post-hepatic venous pressures
  • Reduced hepatic venous drainage
  • Increased venous inflow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Non-pitting oedema caused by myxoedema:
- Association
- How does it cause oedema? (Mucop….)

A
  • Myxoedema is commonly associated with severe hypothyroidism
  • excessive deposition of mucopolysaccharides in the skin/dermis which attract water, leading to swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Lymph has three major functions:
- Protein
- Fat
- Immune

A
  • Return protein and fluid from the extravascular fluid to maintain low protein conc.
  • Aid absorption and transport of fat from the small intestine
  • Immunological role - lymph glands, circulation of immune cells, removal of bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Lymphoedema:
- Definition

A
  • The lymphatic system fails to drain lymph, which accumulates in the tissues, usually arms and legs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Primary lymphoedema:

A
  • A rare genetic condition whereby the lymphatic system fails to develop properly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Secondary lymphoedema:
- Many causes (6)
- s
- R
- C
- I/P I
- I C
- V D

A
  • Basically anything that blocks/damages the lymph nodes
  • Surgery
  • Radiation treatment
  • Cancer
  • Infection/parasitic invasion
  • Inflammatory conditions
  • Venous diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Osmole:

A
  • A unit of osmotic pressure equivalent to the amount of solute that dissociates in solution to form one mole of particles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

OsmolaLity:

A
  • Measure of the osmoles of solute per Kg of solvent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

OsmolaRity:

A
  • Measure of the osmoles of solute per L of solution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Polyuria:
Polydipsia:

A

Polyuria: excessive urine output
Polydipsia: excessive drinking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

SIADH effects:
- Sodium/serum osmolality
- Urine output
- Urine osmolality

A
  • Decrease
  • Decrease
  • Increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Dehydration effects:
- Sodium/serum osmolality
- Urine output
- Urine osmolality

A
  • Increase
  • Decrease
  • Increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Diabetes insipidus:
- Sodium/serum osmolality
- Urine output
- Urine osmolality

A
  • Increase
  • Increase
  • Decrease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

ADH (anti-diuretic hormone): function

A
  • ADH induces expression of water transport proteins in the late distal tubule and collecting duct to increase water reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

ADH: method of action (3 steps)
- acts on …
- Increases water…
- by phosphorylation of….

A
  • Acts on renal collecting ducts via V2 receptors to
  • increase water permeability (cAMP-dependant mechanism)
    *by phosphorylation of aquaporin, which leads to decreased urine formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Causes of polydipsia: (6)
- D I
- D M
- P P
- Hc/E
- D
- U

A
  • Diabetes insipidus
    • Diabetes mellitus
    • Primary Polydipsia
    • Hypercalcaemia/Electrolyte disturbances
    • Diuretics
    • UTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Diabetes insipidus: what is it?

A
  • Disorder of AVP release or action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Diabetes insipidus - signs and symptoms: infants

A
  • Forceful sucking
  • Soaked nappies
55
Q

Diabetes insipidus - signs and symptoms: Young children

A
  • Primary enuresis
  • Toilet training differences
56
Q

Diabetes insipidus - signs and symptoms: older children

A
  • High urinary output
  • Nocturia
  • Tiredness
57
Q

Water deprivation test: Diabetes insipidus is confirmed if: (3)

A
  • Plasma osmolality is rising
  • Plasma Na is elevated
  • Urine osmolality remains dilute
58
Q

What is the cause of DI?: central
- Caused by
- Check for ….
- Other testing (2)
- Isolated ?????

A
  • AVP deficiency
  • Check for other pituitary hormones - ACTH, TSH, LH, FSH, Prolactin
  • GH testing may be required
  • MRI brain
  • Cranial or Central DI is rarely isolated
59
Q

What is the cause of DI?: nephrogenic
- Caused by
- How to test for it

A
  • AVP resistance
  • Genetic testing for mutation in AVP receptor
60
Q

How to clinical test for nephrogenic vs central DI?

A
  • Administer test dose of DDAVP (desmopresin) at the end of deprivation test
  • If urine becomes concentrated = Central DI
  • If no change occurs = Nephrogenic DI
61
Q

SIADH: Signs and Symptoms (2)

A
  • Reduced urine output
  • Reduced sodium (dilutional) = nausea, vomiting, cramps, irritability, rarely seizures
62
Q

SIADH meaning:

A
  • Syndrome of Inappropriate ADH Secretion
63
Q

Causes of SIADH:
- T
- C D
- CN
- D
- R O

A
  • Tumours
  • Chest disease
  • CNS disorders
  • Drugs
  • Reset osmostat
64
Q

Diabetes Mellitus: symptoms
- P
- P
- W
- F
- A
- N

A

· Polydipsia
· Polyuria
· Weight loss
· Fatigue
· Abdominal pain
- Nocturnal enuresis

65
Q

How does diabetes cause these symptoms?
- Polyuria and Polydipsia

A
  1. Increase in glucose
  2. Renal excretion of glucose
  3. Osmotic diuresis with excessive water loss (polyuria)
  4. Dehydration
  5. Polydipsia to compensate
66
Q

Diabetic Ketoacidosis (DKA): How does an insulin deficiency cause acidosis

A
  1. Increased lipolysis
  2. Increased FFA to the liver
  3. Ketogenesis
  4. Acidosis
67
Q

DKA: treatment

A

· Mainstay of treatment:
- Rehydrate with IV fluids gradually over 48 hours
- Treat insulin deficiency with IV insulin
- Close monitoring of clinical condition, electrolyte and glucose levels

68
Q

Diabetes mellitus: treatment

A
  • Insulin
    · Chronic disease management
    · Screening for complications of diabetes
69
Q

Primary Polydipsia:

A

· Excessive fluid intake caused by a behavioural
component
· Often from drinking non-water substances
· Don’t restrict water until DI or DM excluded

70
Q

Psychogenic polydipsia:

A
  • Psychogenic polydipsia: used to describe the association between polydipsia and psychiatric disorders e.g. schizophrenia/anxiety disorders (6-20% prevalence)
71
Q

Diuretics: what do they do? (2)

A
  • They reduce Na+ reabsorption in the tubular nephron, increasing Na+ excretion.
  • An increase in Na+ in the urine increases water excretion by osmosis
72
Q

Diuretics: why are they used? (2)
- Removal of …..
- Combinations of …..

A
  • For the removal of fluid accumulations from interstitial space or the circulation when these have clinical consequences
  • Combos of diuretics can be used to offset potential side effects
73
Q

Osmotic diuresis: two possible principles of action
1. Osmotic diuresis
2. Ion transport modulators

A
  1. Add an impermeable solute to tubular fluid, to reduce H2O reabsorption
  2. Reduce Na+ reabsorption across the tubular membrane
74
Q

Osmotic diuresis - Mannitol
- Method of action

A
  • Filtered at glomerulus and is poorly reabsorbed, raises plasma and tubule osmolarity, reducing loss of Na+ in diuresis
75
Q

Mannitol - Clinically useful characteristics (2)

A
  • Does not enter eye or brain. This makes it useful in the treatment of raised intracranial/intraocular pressure
  • Useful to drain relatively inaccessible oedema accumulations
76
Q

Proximal tubule mechanics:
- Transport
- Flux

A
  • Na+ in the tubule fluid is exchanged for H+, pumping Na+ into the epithelial cell where it is pumped out via an ATP-consuming Na-pump
  • Na+ transport is accompanied by an osmotic flux (H2O) from tubular fluid
77
Q

Carbonic Anhydrase (CA): role in proximal tubule
- Role
- How it does this in simple terms
- Inhibition

A
  • CA catalyses the production of H2O and CO2 from HCO3- and H+
  • It takes the H+ being exchanged for water and makes new water
  • CA inhibition would reduce Na+ reabsorption and hence water re-uptake
78
Q

Carbonic anhydrase inhibitors: Acetazolamide
- Action
- Effects

A
  • Reduces Na+ reabsorption hence H2O reabsorption by suppressing H+ uptake
  • Increases excretion of HCO3- (Na+, K+, H2O), causing metabolic acidosis and mildly alkaline urine
79
Q

What does Acetazolamide treat?:
G
MA
P for AS

A
  • Glaucoma: reduces the formation of aqueous humour
  • Adjunct therapy in metabolic alkalosis
  • Prophylaxis for altitude sickness
80
Q

Mechanics of the ascending loop of Henle:
The concentration of … is generated by (2)

A
  • The concentration gradient of the medullary interstitium is generated by:
    1. An apical Na+/K+/2Cl- co-transporter
    2. A basolateral Na-pump
  • The ascending limb is impermeable to water
81
Q

Loop diuretics: Furosemide
- Action (ascending)
- Aims of action (2)
- End result

A
  • Inhibits the Na+/K+/2Cl- co transporter to:
    1. Reduce the medullary interstitial conc. gradient
    2. Maintain a greater tubule osmolality
  • 20% of water load is usually reabsorbed by action of the co-transporter. Inhibition causes an equivalent water retention, causing a huge urine production increase
82
Q

Loop diuretics: side effects (2)

A
  • Hypovolaemia can occur leading to hypotension (lowered systemic arterial pressure)
  • Loss of tubular fluid can result in hypokalaemia causing muscle weakness and possible ECG changes
83
Q

Loop diuretic side effects: how to avoid hypokalaemia?

A
  • Loss of excess K+ can be ameliorated by using loop diuretics in combination with K+-sparing diuretics
84
Q

K+ sparing diuretics: Spironolactone
- Action
- Clinical use

A
  • Blocks the aldosterone receptor, preventing the loss of K+ into the tubular fluid in the distal tubule
  • This prevents hypokalaemia that can be caused by more powerful loop diuretics
85
Q

K+ sparing diuretics: Amiloride and Triamterene

A
  • Both block epithelial Na+ channels (ENaC), preventing loss K+ from Na+/K+ trade
  • Limited efficacy in generating diuresis, so used in conjuction with stronger loop diuretics as a K+ preserver
86
Q

K+-sparing diuretics: side effects

A
  • Can cause Hyperkalaemia in patients with raised K+ from renal failure or diabetes
87
Q

Renal tubule handling of ions and water:
- Transporter present
- What blocks this?

A
  • Distal tubule cells express a Na+ - Cl- co-transporter that reabsorbs Na+ from the tubular lumen
  • Thiazides
88
Q

Thiazide-like diueretics:
- What are they?
- Action
- Example

A
  • Several compounds that share the same effect but vary in structure.
  • Block the Na+-Cl- co-transporter in the distal tubule , preventing reabsorption of Na+ from the tubular lumen
  • Hydrochlorothiazide is a widely used example
89
Q

Thiazide-like diuretics: side effects

A
  • Hypokalaemia: Same as loop diuretics, thiazide-like diuretics increase urinary K+ losses
  • Hypotension, dizziness and syncope due to hypovolaemia
90
Q

Chronic kidney disease definition:

A
  • Abnormal kidney function for more than 3 months, with implications for health
91
Q

Three common causes of CKD:

A
  • Diabetes
  • Hypertension
  • Obesity
92
Q

eGfR meaning:

A
  • Measures how much blood your glomeruli filters clean every minute based on your body size
93
Q

Clinical utility of eGFR:

A
  • Used to watch for the onset of kidney disease and monitor severity of existing cases
  • > 90 is normal
94
Q

Non-specific advanced CKD symptoms: (5)

A
  • Fatigue
  • Loss of appetite
  • Nausea/vomiting
  • Itchy skin
  • Cramp
95
Q

CKD symptom presentation:

A
  • usually minimally symptomatic
96
Q

Acute Kidney Disease (AKD):

A
  • Abnormal kidney function present for less than 3 months, with implications for health
97
Q

Acute Kidney Injury (AKI):

A
  • Abnormal kidney function present for less than one week, with implications for health
98
Q

acute renal failure: prerenal
- Definition
- Causes (3)

A
  • Sudden and severe drop in blood pressure or interruption of blood flow to the kidneys
  • Diarrhoea, Bleeding, Burns
99
Q

acute renal failure: Intrarenal
- definition
- Causes (3)

A
  • Direct damage to the kidneys
  • Acute tubular necrosis, Drugs, autoimmune
100
Q

acute renal failure: Postrenal
- Defintion
- Causes

A
  • Sudden obstruction of urine flow
  • enlarged prostate, kidney stones, bladder tumour or injury
101
Q

Causes of acute renal failure: prevalence
1. Prerenal
2. Intrarenal
3. Postrenal

A
  1. 70%
  2. 10%
  3. 30%
102
Q

Why can eGFRs not be used for AKD

A
  • It takes a very large change in GFR to result in even a small measurable change in serum creatine (higher regions)
103
Q

Symptoms of advanced AKD:

A
  • Fatigue
  • Loss of appetite
  • Nausea/vomiting
  • Cramp
104
Q

End-Stage Kidney Disease (ESKD): Clinical definition (2)

A
  • GFR < 15ml/min per 1.73m^2
    OR
  • If they are on dialysis/transplant
105
Q

The different names of Kidney failure:

A
  • AK13 if dialysed for AKI
  • CKD5D if dialysed for CKD
106
Q

Kidney functions: (6)
- Remove (1)
- Regulate (4)
- Control (1)

A

-Remove soluble waste products from the blood
-Regulate amount of water in the blood
- Regulate amount of sodium in the blood
- Regulate acidity in blood
- Control calcium and phosphate metabolism
- Regulate blood cell production (produces erythropoietin)

107
Q

Treatment for kidney failure effectiveness: Dialysis

A
  • Only restores removal of waste solutes and Salt/water balance
108
Q

Treatment for kidney failure effectiveness: kidney transplantation

A
  • Restores all kidney functions
109
Q

Typical features of a patient with a surgical atriovenous fistula: (3)

A
  • Purplish bulging veins
  • Swelling in arms/legs
  • Decreased BP/HF
110
Q

Lower UTI: Distinguishing signs

A
  • Nocturia
  • Suprapubic pain
  • NO FEVER
111
Q

Lower UTI: definiton

A
  • Simple cystitis of the bladder/urethra
112
Q

Upper UTI: definition

A
  • Pyelonephritis (complicated infection) of the Aorta/Inferior VC/Ureters/Kidneys
113
Q

upper UTI: distinguishing signs

A
  • Fever
  • Flank pain (renal angle tenderness)
  • Raised heart rate
114
Q

Micro-organisms that commonly cause UTI:

A
  • E. coli (most common)
  • Staphylococcus: colonises the UT and perineum
115
Q

Common risk factors for urinary tract infections: Structural (4)

A
  • Female
  • Pregnancy
  • Abnormal UT (congenital)
  • Malignancy
116
Q

Common risk factors for urinary tract infections: co-morbidities (5)

A
  • Diabetes
  • Immunocompromised
  • Urinary catheter
  • Ureteric stent
  • Previous UT
117
Q

Common risk factors for urinary tract infections: Other risk factors (2)

A
  • Sexual activity
  • Dehydration
118
Q

Signs of UTI on dipstick: (3)

A
  • Raised leukocyte levels
  • Raised Nitrite levels
  • RBC: Haematuria
119
Q

Suspected UTI: when to use a dipstick test?

A
  • Women (under 65) with suspected UTI
  • Infants/children under 16 with suspected UTI
120
Q

When to use Urine cultures: (5)

A
  • Over 65 is symptomatic and antibiotic given
  • Suspected polynephritis or sepsis
  • Suspected UTI in men
  • Urinary catheter in place
  • Failed antibiotics/recurring UTI
121
Q

Nervous control of the lower urinary tract -
bladder: M3 receptors
- Stimulated by
- Innervation type
- Effect

A
  • Stimulated by ACh via the pelvic nerve
  • Parasympathetic (pelvic) nerve
  • Excitatory -> cause muscle contraction
122
Q

Nervous control of the lower urinary tract -
bladder: B3 receptors
- Stimulated by …..
- Innervation type
- Effect

A
  • Stimulated by NA via the hypogastric nerve
  • Sympathetic nerve
  • Inhibitory -> causes muscle relaxation
123
Q

Nervous control of the lower urinary tract -
Urethra: a1 receptors
- Stimulated by…
- Innervation type
- Effect

A
  • Stimulated by NA via the hypogastric nerve
    -Sympathetic nerve
  • Excitatory -> urethra contraction
124
Q

Nervous control of the lower urinary tract -
External urethral sphincter: nicotinic receptors
- Stimulated by
- Innervation type
- Effect

A
  • Stimulated by ACh via Pudenal nerve
  • Somatic innervation
  • Excitatory -> EUS opens
125
Q

The micturition cycles: peripheral nervous system: filling
- General state
- Parasympathetic
- Sympathetic
- Pudenal

A
  • Bladder is relaxed; outflow tract contracted
  • Parasympathetic nerve (S2-S4) inactive
  • Sympathetic nerve (T11-L2) active, maintains bladder relaxation
  • Pudenal nerve (S2 to S4) active, retain EUS closure
126
Q

The micturition cycles: peripheral nervous system: voiding
- General state

  • Parasympathetic
  • Sympathetic
  • Pudenal
A
  • Bladder contracts, outflow tract relaxed
  • Parasympathetic nerve: active, releases ACh, bladder contracts and urethra relaxes
  • Sympathetic nerve inactive
  • Pudenal nerve less active, EUS opens
127
Q

The micturition cycles: Sacral coordination (CNS):
- PMC

A
  • PMC, upon stimulation, leads to detrusor muscle contraction and urethral sphincter relaxation -> urination
128
Q

Measurement of urinary tract function: Frequency-volume chart
- When is it used?
- What does it look at?

A
  • Used in initial assessment for LUT
  • Looks at nocturia, leakage, frequency
129
Q

Measurement of urinary tract function: Ultrasound-bladder scan
- What does it look at
- When is it used

A
  • Looks at residual volume and problems (UTI, CKD), can measure bladder volume
  • Specialist assessment, bladder should void completely
130
Q

Measurement of urinary tract function: Volume-flow measurements

A
  • Filling urodynamics and video-urodynamics
  • If a patient fails to respond to a conservative treatment of drugs
131
Q

Types of urinary tract stones: Calcium stones
- Formation
- Risk factors

A
  • Formed from calcium oxalate / phosphate
  • Risk factors: hypercalciuria, hyperoxaluria and hyperparathyroidism
132
Q

Types of urinary tract stones: Uric acid stones
- Risk factors

A
  • Risk factors: High purine intake or malignancies
133
Q

Types of urinary tract stones: Cystine stones
- Risk factors

A
  • Risk factors: Reduced renal tubular reabsorption of cysteine, ornithine, lysine and arginine
134
Q

Types of urinary tract stones: Struvite stones
- Made of
- Risk factor (bacterial)

A
  • Made of magnesium ammonium phosphate
  • Risk factors: chronic UTI of gram-ve, urease positive organisms

Med Yr2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions