S2SS Flashcards
Kidney:
Label regions of medulla and adipose tissue of hilum
Kidney:
What type of epithelia are the black arrows pointing to?
Options embedded in image
Kidney:
What is the name of the space lined by the epithelia pointed to by the black arrows:
Pelvis
Ureter
Calyx
Which of the following are functions performed by mesangial cells and mesangial matrix?
Participation in the tubuloglomerular feedback mechanism
Structural support of glomerular capillary loops
Secretion of vasoactive factors and cytokines
Phagocytosis
Contraction to control glomerular capillary blood flow
All of the above
Which features are associated wit the proximal convoluted tubule and which are associated with the distal convoluted tubule?
Smaller cells (or ore visible nuclei)
Brush border
Paler cytoplasm
Larger more well-defined lumen
More numerous cross sections per field of view (ie longer tuble that appears more often in sllide)
Proximal convoluted tubule:
Brush border and more numerous cross sections per view
Distal convoluted tubule:
Smaller cells
Paler cytoplasm
Larger more well defined lumen
Label the glomerulus and distal convoluted tubule
Compared with proximal convoluted tubules (PCTs) the distal convoluted tubules (DCTs) are lined by smaller cuboidal cells with slightly paler cytoplasm. PCTs are longer, thus there are more cross sections of PCTs that DCTs in the cortex.
Kidney:
Identify the cell types (as listed in the menu embedded in the image)
Mesangial
Endothelial
Epithelial
Kidney:
Label:
BC
BM
BS
C
E
F
M
MM
P
P1
P2
SPS
BC: Bowman’s capsule
BM: Glomerular basement membrane
BS: Bowman’s space
C: Capillary loop or lumen
E: Endothelial cell (nuclei)
F: Fenestration (in endothelium)
M: Mesangial cell (nuclei)
MM: Mesangial matrix
P: Podocyte (or visceral epithelial cell)
P 1 : Primary foot process
P 2 : Secondary foot process (or pedicel)
SPS: Sub-podocyte space
In which region of the kidney are glomeruli located?
Medulla
Cortex
Cortex
What will happen to nephron tubules associated with a sclerosed glomerulus?
Atrophy
Necrosis
Hypertrophy
Hyperplasia
Atrophy
Efferent arterioles from the glomerulus give rise to the peritubular capillaries and vasa recta. Blood will not flow through sclerosed glomeruli so the remainder of the nephron (i.e. tubules) will undergo ischaemic atrophy. As this is a chronic process it will happen slowly. There will also be associated interstitial chronic inflammation and fibrosis. The kidney will atrophy over time. Renal atrophy can be seen radiologically.
How is a kidney with extensive glomerulosclerosis (and associated tubular changes) likely to appear macroscopically?
Enlarged
Very small
Necrotic
Cystic
Very small
Compare the features of the normal glomerullus vs the two showing a patient with membraneous nephropathy.
Why was this patient tested for antinucelar antibodies, anti-double-stranded DNA and hepatitis B and C?
The patient may have a secondary glomerulonephritis that has developed as a result of another disease process such as hepatits B or C or an autoimmune disease such as systemic lupus erythematosus, where patients have various autoantibodies (e.g. anti- double-stranded DNA) in their serum.
While most cases of membraneous nephropathy are primary or idiopathic, some develop secondarily to other diseases such as hepatitis B and C and SLE, or drugs. Antigens of these other diseases, or circulating immune complexes, deposit in the glomerulus and initiate immune responses.
The immunofluorescent micrographs of the two glomerular disorders (IgA nephrophathy and membranous nephropathy) are presented here to allow direct comparison.
In which glomerular region has the IgA depositied in the section of IgA nephropathy AND In which glomerular region has the IgG depositied in the section of membranous nephropathy
Within the:
glomerular basement membrane
Bowman’s space
mesangium
juxtaglomerular apparatus
cappilary lumen
IgA nephropathy - IgA is deposited within the mesangium
Membranous nephropathy - IgG is deposited within the glomerular basement membrane
Both two forms of glomerulonephritis (membranous and IgA) are the most common types in adults. Membranous typically presents with proteinuria and IgA with haematuria. The patient’s serum creatinine level is frequently normal when first diagnosed. Some patients progress to end stage renal disease. Some patients may present with end stage renal disease having previously been asymptomatic.
What changes would be expected in the kidneys in a patient with end stage renal disease caused by IgA or membraneous nephropathy?
Renal atrophy with glomerular and tubular necrosis
Renal enlargement with hypertrophy of non-diseased glomeruli and nephrons
Renal atrophy with sclerosis of diseased glomeruli and atrophy of associated tubules
Renal atrophy with sclerosis of diseased glomeruli and atrophy of associated tubules
Over time diseased glomeruli will become sclerosed (mesangial expansion in IgA affects blood flow through the glomerulus causing ischaemia; whilst immunoglubins in membraneous nephropathy affect podocytes which produce TGF-β and impaired filtration will result in sclerosis). Tubules secondarily become atrophic and there is interstitial fibrosis. The kidneys macroscpically will appear small and atrophic.
Which of the following pathological processes may be associated with fever? (more than one may be correct)
Acute inflammation
Chronic inflammation
Infarction
Malignancy
All of the above
Fever is caused by the action of IL-1 and TNF, predominantly produced by macrophages in inflammatory responses, on the hypothalamus. Inflammation may be associated with all these pathologic processes. Following infarction there may be mild fever associated with the inflammatory response, and chronic inflammatory responses are associated with malignancy. Certain types of malignancy in particular e.g. lymphomas are especially likely to cause fever. Although in this case, the fever is caused by infection, in many cases it is not
A 42-year-old diabetic female presented with a 24-hour history of fevers and chills with anorexia (loss of appetite), right loin pain, urinary frequency and dysuria.
On examination she looked unwell, was febrile at 39.8°C and had a rapid heart rate. Urinalysis was strongly positive for leukocytes and blood, and moderately positive for protein. The urine sample was cloudy and slightly brownish in colour.
Low and high power micrographs representative of the disease process taking place in the patient’s right kidney are shown below.
What basic pathological process is responsible for this patient’s illness?
Ischaemia/infarction
A malignant neoplastic process
A cellular adaptive change
A benign neoplastic process
An immunological response
Acute inflammation
Chronic inflammation
Acute inflammation
42-year-old diabetic female presented with a 24-hour history of fevers and chills with anorexia (loss of appetite), right loin pain, urinary frequency and dysuria.
On examination she looked unwell, was febrile at 39.8°C and had a rapid heart rate. Urinalysis was strongly positive for leukocytes and blood, and moderately positive for protein. The urine sample was cloudy and slightly brownish in colour.
Low and high power micrographs representative of the disease process taking place in the patient’s right kidney are shown below.
Which part of the kidney is predominantly affected in this patient?
Glomeruli
Tubules and interstitium
Vessels
Tubules and interstitium
A 42-year-old diabetic female presented with a 24-hour history of fevers and chills with anorexia (loss of appetite), right loin pain, urinary frequency and dysuria.
On examination she looked unwell, was febrile at 39.8°C and had a rapid heart rate. Urinalysis was strongly positive for leukocytes and blood, and moderately positive for protein. The urine sample was cloudy and slightly brownish in colour.
Low and high power micrographs representative of the disease process taking place in the patient’s right kidney are shown below.
What is the most appropriate diagnosis?
Cystitis
Glomerulonephritis
Renal infarction
Acute pyelonephritis
Acute tubular necrosis
Acute interstitial nephritis
Chronic pyelonephritis
The patient has acute pyelonephritis.
This results from infection of the kidney. Infection usually reaches the kidney from the bladder in patients with predisposing factors (such as immune suppression, abnormalities of the urinary tract leading to reflux, presence of renal stones, glucosuria, impaired bladder emptying). Occasionally infection may reach the kidneys via the blood. The renal pelvis, tubules and interstitium are infiltrated by neutrophils.
Note that here the acute inflammation (and bacteria) may damage tubules and adjacent blood vessels, leading to haematuria and proteinuria.
42-year-old diabetic female presented with a 24-hour history of fevers and chills with anorexia (loss of appetite), right loin pain, urinary frequency and dysuria.
On examination she looked unwell, was febrile at 39.8°C and had a rapid heart rate. Urinalysis was strongly positive for leukocytes and blood, and moderately positive for protein. The urine sample was cloudy and slightly brownish in colour.
This patient is diagnosed with acute pyelonephritis.
What clinical features suggest this diagnosis rather than cystitis?
While one cannot always distinguish acute pyelonephritis from cystitis on clinical features, cystitis is less likely to be accompanied by loin pain (which suggests acute stretching of the renal capsule) and is less likely to be accompanied by a systemic inflammatory response i.e. fever, chills, malaise etc.
A 74-year-old woman had a long history of hypertension and angina. Despite treatment with an ACE inhibitor and a calcium-channel blocker, her blood pressure was not well controlled. She was referred to a cardiologist with a view to improving her blood pressure control. No underlying cause had been found for her hypertension, and she did not have diabetes.
On examination, she had a slim body habitus, and her blood pressure was 160/96, with vital signs otherwise normal. Her apex beat was found at the 5th intercostal space slightly lateral to the mid-clavicular line and was described as “heaving”. Bilateral basal pulmonary crackles were heard. Urinalysis showed trace proteinuria with no other abnormalities. Fundoscopy showed “silver wiring” and “AV nipping”, consistent with long term hypertensive changes in arteries, but no papilloedema or haemorrhages.
What type of hypertension is she most likely to have?
Primary essential hypertension
Malignant hypertension
Secondary hypertension
Renovascular hypertension
Primary essential hypertension
The patient is most likely to have primary essential hypertension.
Primary essential hypertension is most common, the clinical features are consistent with this, and we are told that no underlying cause of her hypertension has been found (this doesn’t necessarily exclude secondary hypertension but makes it less likely). The blood pressure is not especially high and there is no evidence to suggest acute end organ damage such as acute renal failure or hypertensive encephalopathy i.e. this is unlikely to be malignant hypertension.
Note that the term renovascular hypertension refers to that caused by renal artery stenosis, usually caused by atherosclerosis.
A 74-year-old woman had a long history of hypertension and angina. Despite treatment with an ACE inhibitor and a calcium-channel blocker, her blood pressure was not well controlled. She was referred to a cardiologist with a view to improving her blood pressure control. No underlying cause had been found for her hypertension, and she did not have diabetes.
On examination, she had a slim body habitus, and her blood pressure was 160/96, with vital signs otherwise normal. Her apex beat was found at the 5th intercostal space slightly lateral to the mid-clavicular line and was described as “heaving”. Bilateral basal pulmonary crackles were heard. Urinalysis showed trace proteinuria with no other abnormalities. Fundoscopy showed “silver wiring” and “AV nipping”, consistent with long term hypertensive changes in arteries, but no papilloedema or haemorrhages.
What organs have clinical evidence suggestive of hypertension-related end organ damage?
She has evidence to suggest end organ damage of heart, kidneys and retina.The heaving apex beat suggests left ventricular hypertrophy (LVH), and this is likely to be causing some left ventricular failure as suggested by the slightly displaced apex beat (LV dilation) and pulmonary crackles. The angina is probably related to coronary atherosclerosis or LVH, for which hypertension is a risk factor. Proteinuria may indicate kidney involvement and silver wiring and AV nipping in the retinas are caused by hypertensive small vessel disease.
A 74-year-old woman had a long history of hypertension and angina. Despite treatment with an ACE inhibitor and a calcium-channel blocker, her blood pressure was not well controlled. She was referred to a cardiologist with a view to improving her blood pressure control. No underlying cause had been found for her hypertension, and she did not have diabetes.
On examination, she had a slim body habitus, and her blood pressure was 160/96, with vital signs otherwise normal. Her apex beat was found at the 5th intercostal space slightly lateral to the mid-clavicular line and was described as “heaving”. Bilateral basal pulmonary crackles were heard. Urinalysis showed trace proteinuria with no other abnormalities. Fundoscopy showed “silver wiring” and “AV nipping”, consistent with long term hypertensive changes in arteries, but no papilloedema or haemorrhages.
She died following a myocardial infarction, and, as she was a body donor for the University of Melbourne School of Medicine, her body was embalmed for dissection. On examining her kidneys, the students found that they were slightly small, with a granular surface, and there were several simple fluid filled cysts. The students were intrigued, and they particularly wondered about the microscopic appearance of her renal tissue.
The histological features are typical of which disease process (pick one)?
Renal artery stenosis
Membraneous nephropathy
Benign nephrosclerosis
Renal infarction
Malignant nephrosclerosis
The features in the section are typical of benign nephrosclerosis as occurs with primary essential hypertension.
Examining the kidney cortex section, which features are present that support the previous diagnosis of benign nephrosclerosis? (more than one choice may be correct)
Hyalinised arterioles
Acute inflammation
Patchy tubular atrophy
Crescents
Atherosclerosis
Glomerulosclerosis
Interstitial chronic inflammation and fibrosis
benign nephrosclerosis:
Hyalinised arterioles
Patchy tubular atrophy
Glomerulosclerosis
Interstitial chronic inflammation and fibrosis
A 65-year-old man with a history of ischaemic heart disease presented with haematuria and left loin pain. Investigations included a renal ultrasound which revealed a lesion in his left kidney.
Which of the following may cause haematuria? (more than one may be correct):
Urolithiasis
Acute pyelonephritis
Renal infarction
Certain glomerulonephritic diseases
Bleeding disorders
Cystitis
Urothelial carcinoma
Prostate carcinoma
Renal cell carcinoma
All of them!
A 65-year-old man with a history of ischaemic heart disease presented with haematuria and left loin pain. Investigations included a renal ultrasound which revealed a lesion in his left kidney.
The micrograph is representative of the disease process in his kidney.
Which of the following can be seen in the section? (more than one may be correct)
A cyst
A malignant tumour
Dead and dying neutrophils
Coagulative necrosis
Haemorrhage
A benign tumour
Dead and dying neutrophils
Coagulative necrosis
Haemorrhage
A 65-year-old man with a history of ischaemic heart disease presented with haematuria and left loin pain. Investigations included a renal ultrasound which revealed a lesion in his left kidney.
The micrograph is representative of the disease process in his kidney.
What is the nature of the causative pathological process?
Infection
A metabolic process
An immunological process
A neoplastic process
A degenerative process
Ischaemia
The sections show an area of coagulative necrosis surrounded by haemorrhage and acute inflammation (purple areas around the necrosis in which there are dead and dying neutrophils).
This is an infarct due to acute ischaemia.
A 65-year-old man with a history of ischaemic heart disease presented with haematuria and left loin pain. Investigations included a renal ultrasound which revealed a lesion in his left kidney.
The micrograph is representative of the disease process in his kidney.
What relationship, if any, may his ischaemic heart disease have to the pathology in his kidney? (more than one may correct)
- He may have had an embolism from atherosclerosis in a coronary artery travel to and occlude a branch of a renal artery
- Ischaemic heart disease predisposes to atrial fibrillation -> thrombus formation in left atrium -> thromboembolism occluding a branch of the renal artery
- He may have left heart failure causing reduced renal blood flow
- He may also have atherosclerotic narrowing of his renal artery (in addition to coronary arteries) causing ischaemia to the kidney
- He may have had a myocardial infarction in the past and a thromboembolism from a thrombus in the left ventricle has occluded a branch of the renal artery
- He may also have atherosclerosis in his aorta or renal artery (in addition to coronary arteries) leading to athero- or thrombo-embolism occluding a branch of the renal artery
Wedge shaped renal infarcts such as this are most likely to be due to embolic (athero or thrombo) occlusion of a branch of the renal artery. (NB. The infarct in the section is on the small side and may not have caused symptoms). The artery that is likely to be occluded in this case is probably too small to be occluded by atherosclerosis with thrombosis (remember that atherosclerosis involves large and medium arteries, though can involve smaller arteries in patients with prolonged hypertension or diabetes). Thrombosis may also occur in the setting of vasculitis.
Occlusion of the renal artery itself will result in infarction of the entire kidney (unless there is >1 artery).
Atherosclerotic narrowing of a renal artery will cause chronic ischaemia and potentially atrophy, depending on the severity of narrowing.
Hypoperfusion of the kidney due to heart failure will not result in a focal infarct, but will cause ischaemia to both kidneys. If the heart failure is acute and prolonged, ATN may develop. Chronic hypoperfusion (e.g. in chronic left heart failure) results in renal retention of sodium and water, but is not severe enough to result in atrophy.
An embolus from a coronary artery will get blocked downstream in a smaller coronary artery - it will not travel to the systemic circulation.
A 72-year-old man has been experiencing problems with commencing urination, a weak stream and dribbling for several years. His serum creatinine level is elevated above the reference interval. If he had no other significant symptoms or past medical history, his kidneys are most likely to show (pick one):
Moderate bilateral atrophy
Mild bilateral atrophy and granular surfaces
Dilated calyces and cortical atrophy
Numerous cysts
Coarse scarring at upper and lower poles
Dilated calyces and cortical atrophy:
The patient’s symptoms are suggestive of prostate hyperplasia with obstruction to urinary outflow. This results in urinary retention. When severe, urine can’t drain adequately from the kidney and the pelvis and calyces dilate (hydropnephrosis) with secondary pressure atrophy of the cortex.
Coarse scarring at the poles is suggesitve of chronic pyelonephritis. This results from chronic or recurrent infections which is also a potential complication. It may be asymptomatic but is probably less likely given that we don’t have a history of infection.
A 53-year-old man suffered hypovolemic shock following a motor vehicle accident. He was treated appropriately but his cardiac output remained low for some hours. Over the next 3 days his urine output dropped and there was a marked increase in serum creatinine. A micrograph (high power) showing features representative of the causative disease process in a kidney is demonstrated. What has caused the deterioration in his renal function (pick one)?:
Renal infarction
Crescent formation in Bowman’s space
Patchy necrosis of tubular epithelial cells
Necrosis of glomeruli
Interstitial inflammation
Patchy necrosis of tubular epithelial cells.
The clinical information is consistent with acute tubular necrosis, which is also demonstrated in the micrograph (the proximal convoluted tubules have lost their nuclei).
A 53-year-old woman presented with systemic hypertension. Investigations revealed an underlying renal disease, an example of which is shown in the photograph. This disease is likely to be caused by an abnormality in (pick one):
Tubules
Glomeruli
Renal artery
Intrarenal vessels
Tubules!
This is adult polycystic kidney disease. It results from defects in genes encoding proteins in the cell membranes of tubular epithelial cells. The epithelial cells malfunction, the tubules accumulate fluid and cysts form.
