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Unit 6: LGS > Week 10 > Flashcards

Week 10 Flashcards

1
Q

What are some ways that we can classify kidney disorders?

A
  • Prerenal, intrarenal, & postrenal
  • Intrinsic vs extrinsic
  • Primary vs secondary
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2
Q

which biopsy is most beneficial

A

glomerular diseases, tubular diseases, vascular, interstitial

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3
Q

Acute kidney injury vs chronic process

A
  • sometimes both can happen at the same time
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4
Q

When we’re thinking about prerenal, intrarenal, or postrenal, What is the general approach when trying to figure them out?

  • post; how, sxs, timeline
  • prerenal: what labs could you use
A
  • Pre & post renal: No change in GFR
  • Maybe in post there is an obstruction which you can see w/ US and patient will have low urine output with frequent urgency to urinate; Kinda depends but a lot of times if it is prostate hypertrophy you may see that it developed slowly over time but if it is something else like a stone it may be more acute presentation
  • Creatinine ratio might give you an idea. Fractional excretion of Na+, Signs & sx
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5
Q

How do you start the evaluation of patient who presents with decreased urine ouput

  • hx questions
  • How do we gage the urgency of the situation?
A
  • hx of prostate CA?
  • Volume of urine output/body weight, 24 hr urine collection, US of bladder to look for obstruction, BUN and Cr (need baseline)
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6
Q

• What would be a cut off for this pt where you would be worried about his urine output? When do we diagnose AKI based on urine output?

A

○ Less than about 500mL per day
○ The cut off is .5mL/kg/hr
○ So over the past 12 hrs he should’ve put out 571.8mL at the minimum.

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7
Q

How to get UA with obstruction?

A
  • catheter
  • significant obstruction and sometimes you may not be able to pass a catheter so at that point that is more of an emergency where you would involve the urologist, pt may need to get a stent place or they may be able to scrape some of the internal lining of the prostate to debulk the prostate and get a diagnosis at the same time to confirm it is hyperplasia and not a cancer
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8
Q

Describe the pathophysiologic changes that resulted in post obstructive AKI

  • compensatory mech
  • results in
A
  • if you have an obstructive process you’re gonna increase the pressure w/in the ureter which then increases w/in the nephron. Initially he can have compensatory mechanisms in the arterioles to help maintain GFR, but after a while the increased pressure in the nephron will overrule that and it reduces GFR and affects kidney function
  • At the glomerulus you have high pressure to squeeze blood through that filter and so if you have this increased opposing pressure on bowmans space youre gonna have to offset that somehow so the initial response is dilating afferent arteriole so you can increase the pressure going through there
  • ischemia (decreased perfusion to the tubules so you can end up with ischemic tubular damage), Infection
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9
Q

Predict the following laboratory findings in obstructive AKI

  • Serum creatinine
  • FENa
  • best test
A

○ Serum creatinine: would be elevated. It depends on what phase he is (comp or not). Bc this has been going on for a while and with the really severely decreased urine output it is a good chance that his would be elevated
○ FENa: It can be less than 1 or greater, but in general at the time of diagnosis its gonna be greater than or equal to 1 but its usually not all that helpful
- imaging

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10
Q

If you had obstruction in 1 ureter, why are you not gonna have AKI

A

Usually the other kidney can compensate. Where that is not the case is if you only have 1 functioning kidney and then you get a stone in that kindey, or if you have bilateral stone, but it if is just one side it wont usually cause AKI

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11
Q

What are some of the other causes of post renal azotemia?

A

Stone, BPH, congenital deformities (will show up really early in life), pregnancy, intraabdominal tumors (particularly pelvic - tumors of the uterus, ovaries), lymphoma (abdominal that can cause obstruction bilaterally in the ureters)

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12
Q

Prerenal with motorcycle accident

  • Etiologies
  • causes
  • Patho
  • Diagnostic findings
  • problem
  • imaging
  • Management
A
  • Decreased blood volume due to blood loss or dehydration
  • Hanta virus, post op clot
  • increased blood loss or dehydration –> decreased perfusion of nephron
  • Increased creatinine, increased BUN, decreased urine output; with more impact to BUN so ratio > 20
  • impaired reabsorption –> GFR goes down so you having more reabsorption at the level of the proximal tubule and start having more reabsorption of BUN,
  • to look for intraabdominal bleeding if there was an injury undiagnosed initially
  • Go into OR to stop the bleeding, IV normal 0.9% saline to replace intravascular volume quickly
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13
Q

Intrarenal Etiologies with motorcycle accident

  • drugs
  • management
A
  • Drug induced/antibiotic induced: It would be directly or indirectly toxic to the tubule, Aminoglycosides are the most notorious for this and causing tubular necrosis OR contrast-induced nephropathy
  • Management: Stop antibiotic , Ensure that they’re receiving enough fluids
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14
Q

Postrenal Etiologies with motorcycle accident

A

Trauma that could’ve caused postrenal obstruction

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15
Q

Pt with severe crush injury

  • most likely problem
  • how does this cause injury?
  • results on work up
  • treatment
A
  • rhabdomyolysis
  • increased muscle breakdown and increased serum creatine kinase (surrogate marker for muscle breakdown); You’re also releasing myoglobin –> directly toxic to tubular epithelium
  • Serum creatine kinase, Muddy brown casts
  • Aggressive rehydration for supportive care as they clear out the myoglobin
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16
Q

Pt w/ hx of dementia, BPH, CHF, CKD and diabetes that presents with weakness, dysuria an difficulty passing urine what would happen if this was pre-renal azotemia

  • etiologies
  • Expected diagnostic findings
  • Management
A

○ CHF with decreased ejection fraction could be decreasing perfusion to kidneys; Causes decreased filtration across the glomerulus, Decreased perfusion to everything including the tubules and interstitum
○ Type II diabetes could cause atherosclerosis at the renal artery; Can cause hylaine sclerosis of the renal arteries which decreases the caliper of those arteries and decreases the perfusion as well
○ Dehydration: low BP, dry mucosa; in an older patient it is not very specific; they could have a lot of mouth breathing causing the dry mucosa, but still very important to pay attention to; Patient has said they are so weak they are not getting out of bed, so they are not getting out of bed and oral intake could be another significant problem. This is very important in patients with weakness because it can cause significant dehydration which could be playing into decreased intravascular volume
○ Patient is on ACE i: directly hampers the GFR; Dilates the efferent arteriole and somewhat constricts afferent arteriole
- Elevated BUN/CR and FE Na
- CHF causing renal impairment -> use saline fluids since BP is low; Decrease afterload -> increase CO and increase perfusion to kidneys; Stop ACE inhibitor

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17
Q

Why are ACE inhibitors renal protective?

A
  • progression of renal dx -> decrease in renal mass -> increase in intraglomerular pressure and so we are going to shift the balance and the flow through the glomerulus so you’re going to decrease the GFR to each glomerulus to try and protect it
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18
Q

Pt w/ hx of dementia, BPH, CHF, CKD and diabetes that presents with weakness, dysuria an difficulty passing urine what would happen if this was Post Renal azotemia?

  • etiology
  • management
A
  • BPH: pt has prior history of benign prostatic hypertrophy, so thinking about obstruction
  • put in foley cath ->Monitor output
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19
Q

Pt w/ hx of dementia, BPH, CHF, CKD and diabetes that presents with weakness, dysuria an difficulty passing urine what would happen if this was Intra-renal azotemia?

  • etiology
  • low hgb -> what does this do?
  • dx
  • complications
  • management
A
  • Ischemia associated AKI bc of systemic hypotension ->At some point the pre-renal azotemia becomes severe enough or long standing and shift into intra-renal problem bc intravascular supply problem will lead to ischemic tubular necrosis, etc.
  • CKD causes decreased EPO production which leads to anemia of chronic renal insufficiency -> Exacerbates ischemia bc there will be even lower amount of O2 delivery
  • Elevated creatinine: In a patient with chronic kidney disease will most likely have elevated creatinine at baseline, so would define an acute on chronic renal dx with even higher creatinine than baseline amount
    ○ Bicarb low and K is at high normal -> EKG with peak T waves
  • There are ways you could lower K acutely: give glucose and insulin and shift pathway intracellularly, give bicarb for acidosis but if patient already has EKG changes just take pt to dialysis
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20
Q

Creatinine levels for different stages of AKI

A

□ Stage 1 AKI: 1.5-1.9 X baseline

- Stage 2 AKI: 2X baseline

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21
Q

How does diabetes cause renal damage?

A

Significant intra-renal damage and some degree of pre-renal

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22
Q

What is interplay between AKI and chronic kidney injury

A

Older pt with chronic renal injury are a lot more susceptible and do not recover as fast from acute renal injury from hypoxia, particularly a patient with diabetes, is going to have slower healing response if they do have damage to their tubular epithelium or endothelium so they are already set up for having acute injury. They will have an acute renal injury go to the hospital and get through that but as we talked about in structures last week these acute injuries over time will lead to scarring. You’re damaging more nephrons and scarring them and as you lose those nephrons youre going to cause faster progression of chronic renal dx since damage to these nephrons is irreversible which can then lead to glomerular HTN and these patient will end up on chronic dialysis or renal transplantation.

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23
Q

55 y/o hispanic male w/ severe R flank pain, radiating to RLQ, dysuria, dark colored urine, less urine output, pain of 10/10, emesis. Elevated BP, no fever, unable to sit or lie still

  • what additional tests would you order
  • DX?
  • how could you r/o nephritis
  • Tx?
A
  • UA, CBC, CMP/BMP
  • Kidney stone on R side
  • RBC casts; if there arent any then it is post-renal and problem is happening after glomerulus
  • give IV hydration, pain mgmt (morphine), tamsulosin, and on discharge- catch & analyze stone.
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24
Q

What is leukocyte esterase

A
  • confirms or denies WBC in urine which would indicate or exclude an infection
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25
Q

Can pt have AKI w/ unilateral kidney stone

A
  • No
  • Overall GFR should be maintained though because other kidney is gonna compensate. You define AKI based on urine output or GFR.
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26
Q

Same Pt and at f/u with PCP. Forgot to strain urine and no longer taking meds. Previous hx of diabetes and diet is consistent of high carbs and low veggies, no exercise. BP is elevated, BMI elevated, BUN normal, Cr elevated, Hgb elevated.

  • DX
  • GFR significance?
  • TX
A
  • diabetes
  • Since it was a few days after stone there it could still be from acute episode or could be caused by chronic kidney damage from diabetes but cant make diagnosis yet
  • lifestyle changes because it is first time treating pt
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27
Q

Same pt at a 4 month follow up. Hgb A1C slightly improved but still elevated, BP elevated, weight gain, Creatinine still elevated

  • DX now?
  • staging
  • TX?
A
  • Diabetes, HTN, CKD
  • Stage IIIa CKD with a mild risk of progression
  • Metformin, ACE i,
28
Q

Staging of CKD

A 
○ Stage I is greater than or equal to 90 GFR
○ Stage II is 60-89 GFR
○ IIIa is 45-59 GFR
○ IIIb is 30-44 GFR
○ IV is 15-29 GFR
○ V is less than 15 GFR
29
Q

categories of albuminuria

A
  • A1 is less than 3 mg/mmol (less than 30 mg/g)
  • A2 is 3-30 mg/mmol (30-300 mg/g)
  • A3 is greater than 30 mg/mmol (Greater than 300 mg/g)
30
Q

How does the risk for progression change as we change G or A stage

A

○ Over time those changes in the kidney become irreversible. If we treat with lifestyle modifications and medications it should be reversible. But if we continue this damage to the kidney it’ll cause irreversible remodeling

31
Q

goal for SBP to decrease progression of kidney disease?

- how does that change with hx of diabetes and HTN?

A

• Maximum decrease of risk of progression occurs at SBP goal of 140. You get maximal renal protective effect with a SBP below 140.
- But goal for this pt with CKD, DM, HTN is going to be 120, because this goal ALSO reduces mortality rate and reduces risk for cardiovascular events and stroke

32
Q

When do you refer to a nephrologist

A

Stage III you should refer to nephrologist

33
Q

Benefits to referring to nephrologist early

A
  • help to figure out other disorders that might be contributing
  • help optimize lab tests that you’re going to explore
  • can counsel early, if there is progression, on next steps in terms of renal therapy
34
Q

dietary changes for our pt with CKD

A
  • Decreased sodium
  • Increased phosphate
  • Increase fruit and vegetable intake
  • Minimize EtOH use
  • Optimize fluid intake
35
Q

CKD-Etiology

A
  • DM
  • HTN
  • Atherosclerosis: Chronic vascular insufficiency
  • HIV
  • Hepatitis
  • Lupus
36
Q

Same pt presents 6 month later, compliant with meds, non compliant with lifestyle modifications, BP high, Wt gain, HGB A1C slightly better but still high, Urine microalbumin positive, K elevated, Creatiine more elevated,

  • Plan?
  • staging
  • how would meds change?
  • tx for diabetes
  • long term labs
A
  • EKG to check for peak T waves
  • G3bA2
  • Add a diuretic; specifically thiazide bc of pts hx of kidney stones
  • add insulin
  • HgbA1c, Hgb, Lipids, Electrolytes, PTH, Uric acid, Albumin, Creatinine, GFR, Vitamin D
37
Q

When can you not prescribe a thiazide

A

GFR below 20-30

38
Q

When would you give loop diuretics instead of thiazide

A
  • when elevated K starts to cause changes on EKG (peaked T waves)
39
Q

Why are we worried about Hgb levels with CKD?

A

decreased production of EPO

40
Q

Pt comes back for follow up 2 years later. Stopped diabetes and HTN meds. Feet swelling w/ burning sensation, sxs of poor appetite, nausea, fatigue, palpitations.

  • immediate plan
  • results show peaked T waves, new plan in ED?
  • stage w/ GFR at 14?
A
  • EKG
  • Call for amulance to send to ED, in ED get labs, send to dialysis, referral to nephrologist for long term dialysis
  • stage 5
41
Q

What is an AV fistula? Why is it important?

A

An AV fistula causes extra pressure and extra blood to flow into the vein, making it grow large and strong. The larger vein provides easy, reliable access to blood vessels. Without this kind of access, regular hemodialysis sessions would not be possible.

42
Q
  • 62 yr old, m, w/ right flank pain, 10 lb weight loss, 30 pack yr hs of smoking, tenderness on r CVA, elevated H/H, normal BUN and creatinine, UA w/ hematuria but no protein/glucose/WBC
  • important info
  • DDX
  • tests used
A
  • Right flank pain, 10 lb weight loss over 6 months, Smoker, Blood in urine with nothing else
  • renal stone (can be ruled out with US), pyelonephritis (r/o bc no WBC), renal cell carcinoma
  • abdominal CT or IVP to r/o kidney stone
43
Q

Intravenous pyelogram (IVP)

A
  • x-ray where contrast is injected and then you wait for it to fill the urinary tract so it lights up on x-ray. A stone/blockage will appear dark
44
Q

Why is it significant when a renal tumor invades the vein?

A
  • Renal cell carcinoma has a very characteristic pattern of spreading into the renal vein and ultimately puts you at much greater risk for metastasis once the tumor gets into the vasculature.
  • These tumors tend to present with metastasis fairly early on.
  • Metastasis often goes to lungs, bones, adrenals, and liver.
45
Q
  1. Histo for clear cell renal cell carcinoma

- description

A
  • clustered/grouped cells with stroma in-between, have large, fairly round and regular nuclei that are hyperchromatic (dark), and most importantly, the cytoplasm is clear.
46
Q

Things pathologists should tell you about on their report of histo findings

A
  • A microscopic diagnosis/histopathologic diagnosis

* Staging

47
Q

cytogenetics and genetic abnormalities in clear cell carcinoma

A
  • renal cell carcinomas correlate amazingly well with cytogenetic and genetic abnormalities
  • von Hippel-Lindau gene: lose the gene, have hyper methylation, or inactivation mutations
48
Q

two types of renal cell carcinoma

- which is more common

A
  • sporadic and familial

- sporadic

49
Q
  1. What is this?
    - why do they look so different?
    - what are they covered with? what kind of core?
    - what is in the core?
    - characterisitc feature?
    - cytogenetic/genetic abnormalities in this tumor
    - difference in formation of tumor
A
  • Papillary Carcinoma
  • difference is the plane in which it was cut. Remember that the papilla are like fingers of a hand. The image on the right shows the long finger-like projections as it is cut in the coronal plane. The picture on the left shows the papilla as round circles instead as it is cut in the axial plane.
  • Epithelium w/ fibrous core
  • foam cells
  • psammoma bodies which are round calcium deposits arise from degenerated or necrotic tumor cells that then undergo calcification
  • Genetic= mutated MET, Cytogenetic= trisomy 16
  • Sporadic tumors tend to be solitary and familial tent to be multiple
50
Q

difference in meaning of cytogenic and genetic abnormalities

A

cytogenetic is at the level of the chromosomes and genetic is at the level of the genes

51
Q
  • what is this?
  • Architecture
  • Cell description
  • prevalence
A
  • Chromophobe RCC
  • arranged in sheets (one big plane of tumor cells)
  • Cells are pleomorphic with dense/hyperchromatic chromatin. Nuclei have a little bit of pleomophism as well. Cytoplasm is eosinophilic. You can also see some clearing-out around the nucleus which is known as a perinuclear halo
  • We don’t see this very often. Some chromosomal losses and extreme hypodiploidy can be found in these tumors. But, chromophobe RCC is not commonly seen. Clear cell is what you’ll probably see and maybe some papillary in this patient.
52
Q

Renal Cell Carcinoma Therapy

  • what does it target?
  • how does it work?
  • endogenous agonists
  • signaling cascades affected
  • Inhibitors
  • Why are they used to treat RCC
A
  • receptor tyrosine kinase
  • will be bound -> causes a conformational shape change to dimerize -> undergoes autophosphorylation of the tyrosine amino acid molecule -> down-stream enzymatic activity
  • VEGRF or other epidermal growth factors (EGFs
  • JAK/STAT, MAPK, MAPKK, Akt -> all of these pathways have to do with cell growth, survival, and proliferation
  • Bevacizumab, sunitib, soafenib or pazopanib
  • inhibit things like VEGF and EGFs. By inhibiting multiple growth factors at once, you increase inhibition of all the proliferation cycle. So as you inhibit multiple tyrosine kinases, there is a combined effect of anti-proliferation.
53
Q

5 year old w/ abdominal pain for a month, palpate tender mass in right abdomen, bowel sounds are present, positive for hematuria

  • significance of bowel sounds
  • biopsy of mass would most likely show?
  • description of tumor
  • histo
  • epi and stromal components
  • precursor lesion
  • genetic abnormality
  • treatment
A
  • not GI issue
  • wilms tumor
  • Large, solitary, well-circumscribed mass, in fact pushing the renal parenchyma to the side
  • blastemal stromal endothelial cells
  • epi are arranged in tubules and stroma is eosinophilis w/ loose CT that contain vessels
  • nephrogenic rest: remnants of the embryologic nephrogenic components; which means they are mesenchymal and increases the risk of having a contralateral tumor
  • WT1–for Wilm’s Tumor
  • treatment varies depending on the stage. Increasing stage also increases the duration of treatment & the # of chemotherapy agents that are used at the same time
54
Q

Blastemal elements
- what is it
what do the cells look like

A
  • Very - undifferentiated–nothing distinctive about them, just a bunch of cells
  • very little cytoplasm with blue nuclei
55
Q

Vincristine

A

○ Vinca Alkaloid

○ MOA: M-phase drugs that inhibit microtubule polymerization, Inhibits that mitosis phase

56
Q

Dactinomycin

A

○ Antitumor Antibiotic

○ MOA: Intercalates the DNA– Actually inserts itself within the DNA

57
Q

Doxorubicin

A

○ Anthracycline
○ MOA:§ DNA gyrase–inhibits topoisomerase II
§ O–oxygen free radicals
§ X–cross-linking DNA
§ O–alterations in cell membrane transport:This O represents the cell

58
Q

Etoposide

A

○ Topoisomerase Inhibitor

- MOA = blocks topoisomerase II

59
Q

Cyclophosphamide

A

○ Alkylating Agent

- MOA: Alkylates DNA causing a kink so when DNA gyrase comes in it can’t replicate DNA

60
Q

Urothelial Carcinoma of the Bladder

  • risk factors
  • sxs
  • what is urothelium?
  • PE
  • Lab tests
  • UA
  • Imaging studies
  • Diagnostic tests
A
  • smoking, older individuals, males, exposure to carcinogens, more common in developed countries
  • Painless hematuria, weight loss, fatigue
  • Bladder, ureter, & renal pelvis-> transitional cells
  • most likely normal
  • ↑ lactate, Slight anemia– ↓ H/H, ↑ WBC, ↑ creatinine
  • 2 or 3+ hematuria , ↑ osmolality, + leukocyte esterase
  • CT with & w/o contrast or IVP demonstrate where in the urinary tract the tumor is
  • Urine Cytology: show neoplastic cells; Cystoscopy: Biopsy send to pathology
61
Q
  1. What is this ?

- histo description

A
  • non invasive flat urothelial (transitional cell) carcinoma
  • Not layered, disorganized, pleiomorphic, more basophilic, atypia, increase in number of cells (thickness increased). If this is same magnification, cells are much larger. High N;C ratio. Nuclei very atypical, hyperchromatic. Mitosis also seen
62
Q

How does transitional epithelium differ from stratified squamous?
- umbrella cells

A
  • Cells are in true layers (truly stratified), but when bladder distends with urine, epithelial cells can move and stretch (why they’re called transitional)
  • single layer that protects underlying tissue
63
Q
  1. What is this?
    - key feature
    - difference between R and L
A
  • Papillary carcinoma
  • stromal core that is surrounded by malignant urothelial cells
  • right is very discohesive (cells don’t stick together) , cells are bigger, nuclei are bigger, nuclei are hyperchromatic, pleomorphic cellscategorizing this as high grade; papillary tumor was low grade (pic on left), has mitosis, way too thick, lots of cells, but not as pleomorphic
64
Q

TX of non invasive urothelial carcinoma

A
  • If it’s a large singular tumor that’s not invaded into lamina propria you’d resect it. If invading into lamina propria and there’s multiple tumors, you would inject the BCG therapy; if it was truly in muscle wall you’d have to take bladder out
65
Q

When would BCG be indicated as first line treatment over chemotherapy?

A

When tumor is non invasive, BCG is first line

66
Q

What is BCG?

- How is it administered?

A
  • live bacterium
  • Insertion of catheter in to the bladder so you have attachment of urothelial cells and that will induce inflammation response
67
Q

What else is important about bladder cancer treatment?

A

Our patient has an increased risk of bladder cancer or urothelial cancer anywhere along urinary tract, so they need surveillance (monthly or every 3 months), need urine cytology and cystoscopies/surveillance bc they are truly at increased risk and almost always they get another precursor lesion. So the least toxic treatment we can give them, the better, and we hope to catch these lesions early.

Unit 6: LGS (10 decks)

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