Renal Flashcards
Label this nephron with solutes and what is transported
Bonus points for drugs at each section
Proximal tubule:
NOTE: most reabsorption occurs here
- reabsorbed: sodium, chloride, bicarbonate, potassium, water, glucose, amino acids, urea
- secreted: hydrogen ions, organic acids and organic bases
Thin descending loop of Henle:
- water is reabsorbed
Thick ascending loop of Henle:
- reabsorbed: sodium, chloride, porassium, calcium, bicarbonate ions, magnesium
- hydrogen ions are secreted
Early distal tubule:
- reabsorbed: sodium, chloride, calcium, magnesium, urea
Late distal tubule and collecting duct:
- reabsorbed: sodium, chloride, water and ADH, bicarbonate, potassium
- secreted: potassium, hydrogen ions
Describe the anatomy of the kidney
Retroperitoneal organs: between periitoneum and posterior abdominal wall (psoas and quadratus).
At T12/L3 with hilum at
Anteriorly at ribs 11 and 12.
Helps to identify symptoms of colicky renal pain.
Part of urinary system
Divided into lobes (7/9-18) and segments (apical, upper, middle, lower, posterior)
Key internal anatomy features:
- cortex
- medulla
- columns
- renal sinus
- renal papilla
- capsule
- nephron
- renal pyramid
- munor calyx
- major calyx
- renal pelvis
External anatomy i.e. Covering: fibrous/renal capsule, adipose capsule/perirenal fat, and renal fascia (moving inside to out)
Label the structures of the renal corpuscle
Overall: blood filtering component.
the glomerulus and the Bowman’s capsule: glomeulus is a group of capillaries, fenestrated, supplied by afferent and efferent arteriole.
Filtration.
Filtration barrier: podocytes, BM and mesangial cells
JGA: macula densa, granular and extra-glomeulra cells
Describe the response to dehydration
Antidiuretic Hormone (ADH) MOA
* Dehydration → plasma osmolarity ↑ → osmoreceptors in hypothalamus signalled
* ADH secretion also triggered in hypovolaemia by baroreceptors in carotid sinus and
aortic arch
* ADH - vasopressin synthesised by hypothalamus and secreted by posterior pituitary
* ↑ water retention and vasoconstriction ∴ ↑ BP
* Immediate effect: ADH increases water permeability of collecting duct by osmotic
gradient
* High osmotic gradient = ↑ water permeability of collecting duct, enabling water
to travel from high water concentration within tubule to be reabsorbed into
interstitial space
* 2 players determine homeostatic control:
* Osmocontrol (ADH): hormonal control of NaCl and H2O reabsorption and secretion
* If body preferentially reabsorbs water, extra water dilutes total salt in intravascular and extravascular spaces - when [Na+] ↓,
osmostat in brain senses ↓ Na+ ∴ ↑ salt reabsorption and ↓ water reabsorption
* Delayed effect: increases aquaporin-2 synthesis in principal cells of DCT and CD
Note: severe sqeating: removal of hypo osmotic fluid
* ↓ ECF volume → activation of RAAS → ↑ angiotensin II and aldosterone → Na+ reabsorption
* ↑ plasma osmolality (from ↑ salt loss compared to NaCl loss) → ↑ ADH → ↑ sodium and water reabsorption
What electrolytes changes would you expect in ARF of four days?
High sodium, low sodium , low osmollaliyt, high osmolality, high urates
High sodium, low sodium , low osmollaliyt, high osmolality, high urates
Describe the effect of ADh on plasma and urine osmolarity
ADH increases water and urea permeability of the distal nephron, by upregulating and increasing expression of AQP receptors on apical and basolateral surfaces of cells of distal nephron
- leading to excretion of a small volume of concentrated urine, thereby minimizing further loss of blood volume and decreasing the osmolarity of the plasma back toward normal.
High ADH increases reabsorption of water and produces a low volume of highly concentrated urine; low ADH is associated with a high volume of highly dilute urine.
Describe the consequences and treatment of diabetes insipidus
- rare disorders
- can be congenital or acquired, central or nephrogenic
- results in polyuria, and polydipsia (increased thirst)
- results in decreased release or response to ADH
- before treatment, we would expect that plasma is diluted and thus hypo-osmolar, and that plamsa osmolarity will be increased i.e. hyper-osmolar. This should be confirmed via testing
- administering ADH (if central) will control polyuria, resulting in retention of water. This should increase urine osmolarity and return plasma to normo-osmolarity
- note: risk of hyponatremia
- reduction of solute intake
- thiazide diuretics may also help
Describe the features of the ascending loop, and what solutes are reabsorbed or secreted
cuboidal epithelium in thick limbs (simple?), and squamous over thin limbs. Wide lumen
Thin descending loop of Henle:
- water is reabsorbed
Thick ascending loop of Henle:
- reabsorbed: sodium, chloride, porassium, calcium, bicarbonate ions, magnesium
- hydrogen ions are secreted
Thin ascending limb: squamous epithelial cells don’t have aquaporins ∴
impermeable to water
* Many Na+ and Cl- channels that allow ions to diffuse from tubular fluid into interstitium down concentration gradients
* Interstitial fluid decreases in osmolarity to ~600mOsm/L at top of thin ascending limb
Thick ascending limb: cuboidal epithelial cells - larger than squamous cells (thick)
* No aquaporins ∴ impermeable to water
* Na+/K+/Cl- cotransporter: on apical surface that shuttles 1 Na+, 1 K+ and 2Cl- into the cell
* Target of loop diuretics
* Na+/K+ ATPase: on basolateral surface pumps 3 Na+ into interstitial fluid and 2K+ into the cell
* Na+ and Cl- channels: allow ions to move down gradients
* Volume in tubular fluid < volume in interstitium
* Interstitial fluid becomes more concentrated in medulla
* Countercurrent multiplication: tubular fluid decreases osmolarity up the loop - 325mOsm/L at top of thick ascending loop
Hi
Describe countercurrent multiplication and exchange
Countercurrent multipliers and exchangers
* Countercurrent mechanisms expend energy to create a concentration gradient
* Countercurrent: flow of fluid in opposite directions in adjacent parts of same structure
* Corticopapillary gradient: osmotic gradient from cortex to renal papillae
* Shape allows flow in opposite directions within the same structure
* Deeper in the medulla, the surrounding interstitium is more hypertonic relative to tubule lumen ∴ more water driven out
* Counter current exchanger: vasa recta helps to maintain the osmotic current in the medulla (passive process - no energy required)
* Provides nutrients and takes away waste products without washing away the gradient generated by the LOH via passive process
* Peritubular capillaries permeable to water and solutes
* Along descending limb, water diffuses out of blood into interstitial fluid, whilst solutes diffuse in
* Along ascending limb, extra solutes in the blood diffuse back into interstitium and water diffuses back in
* Water secreted then reabsorbed
* Solutes reabsorbed then secreted
* Because blood flow through vasa recta capillaries is very slow, solutes that are reabsorbed into the bloodstream have time to diffuse
back into interstitial fluid ∴ solute concentration gradient in medulla is maintained
* Counter current multiplier: LOH sets up osmotic gradient in medulla (requires ATP)
* LOH: 2 parallel limbs of renal tubules running in opposite directions, separated by interstitial space of renal medulla
* Descending limb: permeable to water (due to aquaporin), impermeable to solutes
* Water moves into medullary space to make filtrate hypertonic
* Tubule equilibrates with interstitium
* Water moves from tubule to interstitium
* Solutes diffuse from interstitium to tubule
* Ascending limb: impermeable to water, but permeable to solutes
* Na+/K+/2Cl- cotransporter: active transport into medullary space making filtrate hypotonic (via Na+/K+ ATPase gradient) -
tubular fluid diluted
* Interstitium becomes hypertonic, thereby attracting water ∴ multiplies the osmotic gradient between tubular fluid and interstitial
space
* Flow of fluid creates a gradient with ~1200mOsm at inner medulla and ~300mOsm/L in outer cortex
Describe the mechanism of action of furosemide
Furosemide is a loop diuretic. An example of non-acute management – withhold in renal impairment
They work at the ascending loop of Henle (Thick AL), blocking the Na K 2Cl symporter.
This significantly blocks Na reaborpion, decreasing paracellular diffusion. Na retention leads to water retention and increased urine frquncy? and volume.
Available orally and intracenously, greater bioavailbility in IV
Adverse effects, contraindications, indications:
- Indications: edema, forced diuresis, impending anuria, congestive heart failure
- Adverse effects: loss of electrolytes (hypokal, hypergly/uricaemia), uric acid excretion changes, inc in chold and TG, GI disturbancse
- Contraindications: coma hepaticum, anuria; ACEI and NSAID leading to ‘triple whammy’: reduced renal perfusion and AKI, allergies
Describe the mechanism of action of diuretics, indications, side effects and examples
Describe the blood supply to the kidney
Aorta
Renal artery (recall left longer vein, right longer artery)
Segmental Arteries
Interlobar arteries
Arcuate arteries
Interlobular arteries
Afferent arteriole
Glomerular capillary
Efferent arteriole – vasa recta—interlobular/arcuate
peritubular capillaries
Interlobular vein
Arcuate vein
Interlobar vein
Renal vein
IVC
bite/l 5 areas of renal blood supply correspond to five segments: apical, ant sup, ant inf, caudal and post–> help Id vessel involved to localised infarct/nectosis
Compare and contrast metabolic and respiratory acidosis
Respiratory
- A result of abnormal Pco2
- Lung disease, hypoventilation, hyperventilation
- A result of something other than abnormal Pco2
- A high-protein diet, a high-fat diet, heavy exercise, excessive vomiting, severe diarrhea
Describe the role of the kidney in acid base balance
- Acid balance must be maintained for life, within narrow range i.e. 7.35 to 7.45
- 25%
- Other mechanisms include respiratory system and cellular buffering
- Slowest of mechanisms
- Alkalosis and acidosis affect activity of H K to either increase or decrease H abrosption or secretion
- Acidosis: Ammonia synthesis, bicarbonate synthesis
- Receptors involved: Na/H, Na/K/ATPase, Na/3HCO3, Cl/HCO3, H ATPase (Na NH4*, HK ATPase)
- Alkalosis: H retention, and bicarbonate secretion – which occurs ONLY in alkalosis
- Receptors involved: CL/HCO3, Na/glutamine, Na/H, H ATPase, Na/3HCO3, GLUT, Na/K ATPase
Compare and contrast nephritic and nephrotic disease
bonus points: investigations
Recognise – exist on spectrum of disease e.g. sle
Proteinuria in both, more characteristic of nephrotic
Nephritic:
Inflammatory markers
- very sick patients [“dying”]
- decreased urine output (oliguria, anuria)
- haematuria (+/- RBC casts, and dysmorphic RBCs)
- hypertension (kidney detects low GFR, activates RAAS)
- azotemia
- variable proteinuria, typically mild to moderate
Pathology: increased cellularity, due to infiltrate, swollen and damaged endothelial cells, formation of crescents (?), “clogged sieve”
e.g. anti GBM disease, PSGN, IhA (although sacly), MGN, GN
Nephrotic:
- proteinuria > 3.5 g/d
- hypoalbuminaemia secondary to prtiteinuria
(defined byabove)
- oedema (Reduced oncotic pressure)
- hyperlipidaemia (loss of ptotein increases protein poductin in liver, includes LPs)
- infection
- hypercoaguability (LOSS OF at ii IN URINE)
Pathology: flattened/detached podocytes aka damaged to filtration barrier, mesangial changes, faulty BM, leaky sieve
e.g. mi change disease, amyloidosis, diabetic nephropathy, membranous nephropathy
Side note: Investigations
EUC
Urine MCS
Urine albumin
Urine glucose
Complement levels
C3 particularly, often do C4 too however
Antibodies
ASOT (ANTISTREPTOLYSIN O TITRE)
Anti-Dnase B Ab
Glomerulonephritis biopsy
Describe PSGN, its clinical presentation and pathology
This is a prototypical glomerular disease of immune complex etiology.
It usually appears 1 to 4 weeks after a strepto-
coccal infection of the pharynx or skin (impetigo). Skin
infections are commonly associated with overcrowding
and poor hygiene. Poststreptococcal glomerulonephritis
occurs most frequently in children 6 to 10 years of age, but
children and adults of any age can also be affected.
It is a nephritic syndrome. Immune complexes are circulating antigen or planted antigen.
Only certain strains of group A β-hemolytic strepto-
cocci are nephritogenic, more than 90% of cases being
traced to types 12, 4, and 1, which can be identified by
typing of the M protein of the bacterial cell walls. SpeB) as the principal antigenic
deter minant in most but not all cases of poststreptococcal
glomerulonephritis. This protein can directly activate complement, is commonly secreted by nephritogenic
strains of streptococci, and has been localized to the “hump-
like” deposits characteristic of this disease. At the outset, the inciting antigens are exogenously planted
from the circulation in subendothelial locations in glomer-
ular capillary walls, leading to in situ formation of immune
complexes, where they elicit an inflammatory response.
Subsequently, through mechanisms that are not well
understood, the antigen-antibody complexes dissociate,
migrate across the GBM, and re-form on the subepithelial
side of the GBM.
Appears on light microscopy with diffuse endocapllary proliferation, leukocyte infiltration; fluorescence shows IgG and C3, granular, in GBM and mesangium, sometimes IgA; em shows primary subepithelial humps, and subendothelial deposits in early disease stages.
In the typical case, a young child abruptly
develops malaise, fever, nausea, oliguria, and hematuria
(smoky or cola-colored urine) 1 to 2 weeks after recovery
from a sore throat. The patients have dysmorphic red cells
or red cell casts in the urine, mild proteinuria (usually less
than 1 gm/day), periorbital edema, and mild to moderate
hypertension. In adults the onset is more likely to be atypi-
cal, such as the sudden appearance of hypertension or edema, frequently with elevation of BUN. The glomerulo-
nephritis is subclinical in some infected individuals, and is
discovered only on screening for microscopic hematuria
carried out during epidemic outbreaks. Important labora-
tory findings include elevations of antistreptococcal anti-
body titers and a decline in the serum concentration of C3
and other components of the complement cascade.
More than 95% of affected children eventually recover
renal function with conservative therapy aimed at main-
taining sodium and water balance. A small minority of
children (perhaps fewer than 1%) do not improve, become
severely oliguric, and develop a rapidly progressive
form of glomerulonephritis (described later). Some of the
remaining patients may undergo slow progression to
chronic glomerulonephritis with or without recurrence of
an active nephritic picture. Prolonged and persistent heavy
proteinuria and abnormal GFR mark patients with an unfa-
vorable prognosis.
In adults the disease is less benign.
Discuss investigation results in PSGN
C3 is typically low due to its consumption in inflammatory reaction. C4 usually normal.
High creatinine and low GFR
Haematuria present
Positive for anti-C3 on immunofluorescence., also IgG and IgM. Anti-IgG appears granular, characteristic of circulating and in situ immune complex nephritis
deposits located in subepithelial spacw
Glomerulus: neutrophil and other inflammatory cell infiltrate: “busy”
- trapped/extrinsic antigen “c” complexes:
- clumpy
- will deposit in different areas because of size and charge
- +/- complement consumption
Discuss PSGN pathophysiology
PSGN is a nephritic syndrome.
Pathophysilogy is immune complex mediated, circulating or planted antigen
Immune complexes contain streptococcal atigens and specific antibodies which are formed in situ.
Only certain group A beta-haemolytic streptococci are nephritogenic
Can be identified by serotyping M protein
Can be detected by granular appearance of anti-aIgG immunofluorescence
Complement levels: C3 low, C4 low
ASOT: high or positive – recent infection
UEC: high creatinine slightl high Na, low eGFR
Urine: haematuria, albumin
Biopy- disordered, “busy” neutrophils, diffuse endocapillary proliferation
EM- subepithelial humps, subendothelial deposits in early disease stages
List types of glomerulonephritis and provide examples
- Primary or idiopathic - isolated to kidney: may represent immune reaction against intrinsic renal antigen
- Secondary or systemic cause: may represent immune reaction against various antigens- glomerulus may trap antigens/antibody-antigen complexes, leading to glomerulonephritis
- infections (viral/bacterial/parasitic) or post-infectious
- malignancy (Solid organ paraneoplastic or haematolymphoid, amyloidosis)
- drugs (abuse, medical) and toxins (e.g. bites)
- connective tissue disorders and autoimmunity
- systemic vasculitis
- endocrine (diabetes mellitus)
- inflammatory e.g. sarcoidosis
- pregnancy
The disease is immunological; representing a type III hypersensitivity reaction. The exact mechanism by which PSGN occurs is not fully determined. The body responds to nephrogenic streptococcal infection by forming immune complexes containing the streptococcal antigen with a human antibody.[2] Some theories suggest that these immune complexes become deposited in kidney glomeruli reaching through the circulation. Others claim that the condition results from an “in situ” formation of the antigen-antibody complex within the kidney glomeruli. This “In situ immune complex formation” is either due to a reaction against streptococci antigens deposited in the glomerular basement membrane or, according to other theories, due to an antibody reaction against glomerular com¬¬-ponents that cross-react with streptococcal antigen due to molecular mimicry.[5]
The presence of immune complexes leads to the activation of the alternate complement pathway causing infiltration of the leukocytes, and proliferation of the mesangial cells in the glomerulus thus impairing the capillary perfusion and glomerular filtration rate (GFR). Reduction in GFR can lead to renal failure (oliguria or anuria), acid-base imbalance, electrolyte abnormalities, volume overload, edema, and hypertension.
Describe the signs and symptoms of dehydration
- thirsty
- dry mouth
- tachypnoea
- tachycardia
- febrile
- headache
- anuria or oliguria
- hypotensive
- dry mucosal membranes, lips, mouth
- turgor
- irritable, drowsy, or confused
- swollen feet
- flushed skin
- dark coloured urine
- muscle cramps
- fatigue
Describe how creatinine clearance is calculated
U*V /P, urine concentration, urine volume, plama concentration
Describe clearance of PAH and its relevance
eRPF = (urine concentration of PAH) x (urine flow rate/plasma concentration of PAH) = clearance of PAH
Clearance of para-aminohippuric acid depends both on filtration in Bowman’s capsule and secretion into the proximal tubule by organic anion transporters on the basolateral membrane. If PAH plasma concentrations exceed the transport capacity of the organic anion transporters, not all plasma will be cleared of PAH. This results in decreased PAH clearance and underestimation of the renal plasma flow.
Explain the relevance of the ESR and CRP
- CRP measures plasma protein produced by liver cells in response to acute inflammation or infection
- ESR erythrocyte sedimentation rate, also indicates inflammation, but indirectly – effect of several acute phase proteins
- ESR determined by fibrinogen
- also elevated n malignancy, autoimmunity depending on circumstances
Define filtration fraction and RBF
Filtration fraction
The filtration fraction (.FF) is the portion of plasma that is filtered across the glomerulus relative to the renal plasma flow (RPF). Normally about 20%.
RBF estimate calculations
RPF / 1 − hematocrit .
Describe the effect of blood flow on filtration
renal blood flow and GFR normally change in parallel, any increase in renal blood flow causes an increase in GFR. The increased renal O2 consumption (GFR) is offset by an increase in renal oxygen delivery (renal blood flow). This results in a constant arteriovenous O2 difference across the kidney.
Increased blood volume and increased blood pressure will increase GFR.
Describe acid base disturbance in renal failure
Metabolic acidosis occurs with both acute and chronic renal failure and with other types of renal damage. The anion gap may be normal or may be elevated. A generalisation that can be made is: If the renal damage affects both glomeruli and tubules, the acidosis is a high-anion gap acidosis.
Describe bicarbonate synthesis
- all HCO3 is essentially reabsorbed
- modulated by hydrogen ion/ proton secretion
- additionally, it is regulated by H concentration gradient: more H, more efficient
- activity and expression of key H and HCO3 transporters is also regulated and affects efficiency e.g. by acidity levels
- h2co3 formed
- ca on tubular side, results in co2 formed
- h2co3 reformed in cell
- ca leads to regeneration of hco3
- na/hco3 and cl/hco3 export HCO3 into blood
- Note: Na/K/ATPase contributes to exchanger function
- in acidosis (secretion is favourable, therefore) increased H- ATPase in collecting duct, and Na/H antiporter and Na/3HCO3 expression and activity is increased in proximal tubule
- in alkalosis (retention is favourable, therefore) the reverse effects, decreased H-ATPase in collecting duct and decreased Na/H and Na/3HCO3 expression and activity ^[in addition to any other effects?]
- Occurs only in alkalosis
- So that H is retained to buffer high pH and return to baseline
Describe in detail the histology of the kidney
The coverings of the kidney:
- Renal capsule
- Perirenal fat
- Renal fascia
Cortex: grainy appearance as it contains ovoid and coiled parts of the nephrons, receives 90% of kidney blood supply so it appears darker than the medulla
Medulla: appears striped as it contains verical nephron structures. It consists of renal pyramids separated by renal columns. Renal lobes and lobules.
Glomerular capsule: the renal corpuscle is the filtration apparatus – contains glomerulus and glomerular capsule. The kidney filtration apparatus is formed by three layers of tissue; endothelium of the glomerular capillaries, glomerular basement membrane (GBM) and podocytes (visceral layer of renal capsule). Glomerular capillaries are composed of fenestrated endothelium. Fenestrations function as pores. The GBM is more complex than other epithelial basal membranes. It consists of three layers; a thick central lamina densa and two thinner layers (lamina rara interna and lamina rara externa). Inner visceral layer of the glomerular capsule, is made of special cells called podocytes. Podocytes cover the walls of glomerular capillaries, interdigitating with each other and forming narrow slits between their projections. The outer parietal layer is made of simple squamous epithelium and is continuous with the nephron tubules. Together, these three layers function as a selective filter, allowing only molecules below a certain size, and of a certain charge, to pass from the blood and enter the renal tubular system. For example, blood cells, platelets, some proteins and some anions are prevented from leaving the glomerular capillaries, while water and solutes pass through. The remaining unfiltered blood is carried out of the glomerulus by the efferent arteriole, and passes back into the venous system
Pct: composed of simple cuboidal epithelium, rich in mitochondria and microvilli (brush border). This morphology is adapted to the proximal tubule function of absorption and secretion. More than half of the previously filtered water and molecules are returned to the blood (reabsorption) by the proximal tubules.
Nephron loops: Both limbs are composed of simple squamous epithelium. The cells have few organelles, little to no microvilli and low secretion abilities. The two limbs work in parallel, with the surrounding vasa recta capillaries, to adjust the filtrate’s salt (e.g. sodium, chloride, potassium) and water levels. More specifically, the descending limb is highly permeable to water, less permeable to solutes, while the ascending limb is the opposite.
Distal: Both parts of the distal tubule are composed of simple cuboidal epithelium, similar in morphology to the proximal tubule.
A key difference between them is that the epithelium of the distal tubule has less well-developed microvilli. Reabsorption and secretion occurs here, albeit to a lesser degree than in the proximal tubule. By having lots of mitochondria the straight distal tubules can reabsorb any useful substances (electrolytes), and secrete any remaining waste products using active transport. Of particular note is the absorption of sodium, under the regulation of aldosterone.
Collecting system:
They are made of epithelial cells, which get progressively taller as the ducts get larger.
* Cortical collecting ducts - simple cuboidal epithelium
* Medullary collecting ducts - simple columnar epithelium
* Papillary ducts - simple columnar epithelium
Two additional types of cells are distinguishable in these ducts. The principal cells, which are pale staining and play a role in ion transport. Darker staining intercalated cells are scattered amongst the principal cells and are responsible for acid-base balance. Collecting ducts are the last chance site for water and electrolyte reabsorption from the filtrate further concentrating the urine, particularly under the influence of antidiuretic hormone (ADH). No more reabsorption takes place past the medullary collecting ducts.
JGA:
It is formed by 3 types of cells; macula densa, juxtaglomerular granular (JG) cells and extraglomerular mesangial (Lacis) cells.
The macula densa are located in the wall of the distal tubule, at the point where the tubule comes in contact with the glomerulus. Here the regular cuboidal epithelium of the distal tubule crowd together and become columnar in shape. The juxtaglomerular granular (JG) cells are modified smooth muscle cells found surrounding the afferent, and sometimes efferent, arteriole. The third cell type of the JGA are the extraglomerular mesangial (Lacis) cells. These are located in the triangular space between the afferent and efferent arterioles.
What information can be obtained from electron microscopy
Electron microscopy
- detects cellular components/aka the ultrastructure
- looks for podocyte flattening (e.g. in minimal change disease)
- measures thickness of the basement membrane
- looks for deposits
- subendothelial
- intramembranous
- subepithelial
- mesangial
Calculate the clearance of urea and creatinine, and explain why inulin is different
Urinary inulin clearance is considered the gold standard for measuring GFR because inulin has all the properties of an ideal marker. It is freely filtered by the glomerulus, is not secreted or reabsorbed in the tubules, and is not synthetized or metabolized by the kidney.
Because inulin needs to be injected, inulin clearance is not routinely measured. Instead, clinicians monitor creatinine and determine creatinine clearance. The 24-hour urine collection that the patient had done was used to determine creatinine clearance
Compare and contrast cortical and juxtamedullary nephrons
Compare and contrast male and female urethra
note also two curvatures in male: subpubic, upward and concave and prepubic, concave and downard
Clinical Significance:
Two curvatures make males harder to catheterise
Short, straight urethra close to perineum makes females more prone to UTIs
Define AKI and list the tyoes
Prerenal:
Fluid loss (types of shock)
Renal artery stenosis or embolus
Drugs (NSAIDs, ACEIs, ARBs)
Intrarenal:
Glomerulonephritis
Ischaemic/toxin mediated damage to tubules
Acute Interstitial nephritis
Postrenal:
Compression: Tumours, BPH
Obstruction: Kidney Stones
Both cause reduced pressure gradient in glomerulus → azotaemia, epithelial damage
Breakdown the interpretation of ABG, with some breakdwon of causes of NAGMA vs HAGMA metabolic acidosis
HIHIHIHi
Label teh glucose absorption curve and describe its features
- High concentration = high
filtration - Reabsorption is saturable
- After saturation [CHOurine] is
proportional filtered CHO
(minus reabsorption) - Splay phenomenon = gradual
change
Describe the consequences of the triple whammy
