Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology Sp 16 > Exam 2: Diseases 2 > Flashcards

Exam 2: Diseases 2 Flashcards

(95 cards)

Start Studying
1
Q

What is anemia?

What does anemia cause?

A

anemia: Dec red cell mass (RBC and hemoglobin)

anemia causes SOB, weakness, fatigue, pallor

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

What is intravascular hemolysis?

what is extravascular hemolysis?

A

Intravascular: destruction of RBCs within circulation
extravascular: destruction of RBCs within reticuloendothelial system: tissue macrophages of spleen and liver

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

What does extravascular hemolysis lead to

A

DEC haptoglobin, Hyperbilirubinemia and reticulocytosis

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

Hereditary spherocytosis is what kind of hemolysis defect? what is hereditary spherocytosis and what helps relieve the anemia caused by it?

A

Hereditary spherocytosis is a INTRINSIC membrane defect. an abnormality of spectrin leading to less deformable RBCs that can squeeze thru splenic sinusoids so they are sequestered and destroyed in the spleen. a splenectomy helps relieve the problems but RBCs remain abnormal shaped

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

what is a intrinsic defect that is autosomal codominant inheritance? what does it protect from when in a heterozygous state

A

Sickle Cell anemia

heterozygous state protective against malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are two leading causes of ischemia related death for sickle cell anemia pts

A

Acute chest syndrome and stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is a point mutation gene deletion, that is a defect in the synthesis of alpha or beta global chains leading to dec global production and ineffective EPO in bone marrow?

A

Thalassemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the anemia associated with Thalassemia.

what are the target cells of thalassemia? what people is Thalassemia common in?

A

Thalassemia - microcytic, hypochromic anemia that has target cells of basophilic stippling
Common is Mediterranean, African and Southeast Asian decent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what two diseases are protective against malaria

A

sickle cell: heterozygous state

Thalassemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does Thalassemia lead to that may show up in the mouth

A

skeletal deformities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a X linked inheritance that causes RBCs susceptible to oxidant injury, where oxidized Hb denatures and attaches to RBC membrane

A

Glucose 6 Phosphate Dehydrogenase Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a clinical hallmark of Glucose 6 Phosphate Dehydrogenase deficiency?
Intravascular or Extravascular hemolysis

A

G6P Dehydrogenase deficiency = BITE cells

Extravascular hemolysis in spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is an Extrinsic defect autoimmune: occurs in uteri, that is blood group incompatibility

A

Hemolytic disease of newborn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the hallmark of autoimmune hemolytic anemia

A

Spherocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What indicates hemolysis due to mechanical trauma

A

Schistocytes (RBC fragments)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most common basis of anemia worldwide

A

Iron Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the lab results of iron deficiency anemia

A

Microcytic (Low MCV RBCs), hypochromic, DEC serum ferritin, DEC serum iron
Absent reticulocyte response
INC serum Fe binding capacity

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

what is caused by autoABs to parietal cells and IF, what is this associated w

A

Pernicious anemia

Associated w loss of gastric parietal cells, achlorhydria and deficient IF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is a disease where bone marrow is replaced by tumor or fibrosis and you see teardrops RBCs as well as DEC in platelets

A

Myelophthisic Anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is an INC in RBC mass

A

Polycythemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does relative polycythemia cause

A

dehydration and diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does absolute polycythemia cause
Primary?
Secondary?

A

Primary: neoplastic proliferation of RBCs
SecondaryL INC EPO production caused by cyanotic heart disease pulmonary disease, living at high altitudes EPO producing tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is taken up by bones and developing teeth- competing with Ca and interfering w remodeling process produces ? lines on x ray?

A

Lead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does Lead do in the mouth

A

Pb= gingival hyperpigmentation = lead line of soft tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what kind of anemia develops bc of Lead? | What is a hallmark sign of lead poisoning?
Lead= microcytic and Hypochromic anemia | Lead poisoning = wrist drop and footdrop
26
what is the CDC threshold level for concern for Lead? | when is chelation therapy started?
5 micrograms or more | chelation therapy= 45 or greater micrograms
27
what does lead do to the Gi tract? kidnys
Lead causes colicky pain, severe not localized in GI tract | Lead causes damage to tubules, fibrosis, renal failure in kidney
28
use of ecstasy is associated with what?
E (ecstasy)= bruxism
29
what is common when 20% or more of body is burned
Massive fluid shifts= hypovolemia infections: Pseudomonas and Candida electrolyte and nutrition lost
30
Hypothermia causes what
bradycardia, atrial fibrillation and loss of consciousness at cellular level= crystalization of water vasoconstriction, edema, long term causes atrophy and fibrosis
31
what does acute radiation syndrome include describe each phases time frame and symptoms
hematopoietic (2-10 sv, Dec WBC hair loss, infections, sepsis, bleeding and death in 2-6 weeks GI: 10-20 sV = vomitting, bloody diarrhea, shock, sepsis, death in 5-14 days Cerebral: 50 sV, listlessness, drowsiness, seizures, coma, death in 1-4 hours
32
2 disorders of Protein energy malnutrition describe each
Marasmus= deficiency in calorie intake, use proteins fro energy depletes somatic protein compartment, extremities appear emaciated, head is large Kwashiorkor: deficient in proteins, found in Africa and SE asia, depletes visceral protein compartment, weight is between 60-80% of normal but misleading bc of edema
33
2 functional protein compartments | when weight falls to below 60 %of normal child has what?
somatic= skeletal m, marasmus visceral: liver= kwashiorkor weight below 60% of normal= marasmus
34
what disease causes skin changes of alternating zones of hyper and hypo pigmentation w desquamation and causes an enlarged fatty liver
Kwashiorkor
35
what causes elevated BUN and creatinine levels due to DEC GFR
azotemia
36
what is azotemia plus other symptoms like gastroenteritis, peripheral neuropathy, dermatitis, acidosis, pericarditis, hyperkalemia
uremia
37
what is a major clinical renal syndrome that causes proteinuria (mild/ moderate), hematuria, hypertension
acute nephritic syndrome
38
what causes severe proteinuria (over 3.5 grams per day), low serum albumin, anasarca, high serum lipid, lipiduria
Nephrotic syndrome
39
What are two congenital cystic renal diseases
``` autosomal dominant (adult) polycystic kidney disease autosomal recessive (childhood) polycystic kidney disease ```
40
what causes autosomal dominant (adult) polycystic disease
mutation in PKD 1 gene in chromosome 16, that causes a defective protein called polycystic 1
41
what does autosomal dominant (adult) polycystic kidney disease cause in a pt? incidence of disorder
causes UT hemorrhage, pain, gradual onset of renal failure in affected adult affects 1: 500to 1000 persons
42
What is the significant pathology result of Autosomal Dominant Polycystic kidney disease?
Saccular (berry) aneurysms affecting circle of Willis
43
What is the gross pathology of Autosomal dominant Adult polycystic kidney disease? Clinical symptoms of it?
Pathology: large kidneys w numerous cysts at all levels of nephron Clinical signs: flank pain around 4th decade, hematuria, hypertension and UTI, renal failure
44
what is the sudden onset of azotemia with oliguria/ anuria called?
acute renal failure
45
What gene mutation causes Autosomal Recessive Childhood polycystic kidney disease? affected protein? Incidence?
Childhood Polycystic disease = recessive = mutation of PKHD1 gene!! Affected protein = fibrocystin occurs 1:20,000 live births
46
describe what happens with autosomal recessive (childhood) polycystic kidney disease. What is the time frame for this
Numerous uniform sized cysts arise from collecting tubules causing fibrosis and renal failure shortly after birth to several years of age
47
What are the 3 mechanisms of Glomerular disease
1. Immune complex deposits in GBM or mesangium 2. anti GBM AB 3. epithelial and endothelial cell injury
48
What is a glomerular disease thats most obvious clinical sign is severe edema, also causes heavy proteinuria, hypoalbuminemia, hyperlipidemia, and lipiduria
Nephrotic syndrome: most obvious clinical sign is severe edema!
49
nephrotic syndrome is caused by an INC in glomerular capillary permeability to plasma proteins, what 4 things cause nephrotic syndrome
minimal change disease, focal segmental glomerusclerosis, membranous nephropathy, and Nodular glomerularsclerosis (aka diabetes)
50
What is the most common cause of nephrotic syndrome in children, 2/3 of all cases? what is the tx for this?
Minimal change disease treated by corticosteroids
51
Minimal Change disease has what pathology for the LM? IF? EM?
LM: normal appearing glomeruli IF: no immune complex deposits EM: foot process effacement
52
what is a common cause of adult nephrotic syndrome that has poor response to corticosteroid tx? what may this disease be?
Focal segmental Glomerulosclerosis may be primary or secondary to other glomerular diseases w some cases being familial
53
Pathology of focal segmental glomerulosclerosis for LM? IF? and EM
LM: focal and segmental sclerosis w obliteration of capillary loops IF and EM: no immune complex deposits in primary forms
54
What cause of nephrotic syndrome may be primary or secondary to infection, malignancy, SLE, or drugs and has a poor response to corticosteroid tx? who is this disorder most common in
Membranous Nephropathy | most common in adults, may affect children
55
what is the pathology of membranous nephropathy of LM? IF? EM?
LM: normal IF: immune complex deposits EM: deposits in sub epithelial side of GBM
56
What is second to MI as cause of death from diabetes?
renal failure
57
What are the clinical changes seen with diabetes?
hyaline arteriosclerosis atherosclerosis nephrosclerosis
58
What is characterized by acute onset of hematuria, oliguria and azotemia and hypertension
nephritic syndrome
59
what is the result of proliferation of cells within glomeruli accompanied by inflammatory cells severely injuring capillaries walls in nephritic syndrome
nephritic syndrome results in blood passing into urine as well as reduced GFR
60
what are the two causes of nephritic syndrome
acute post infectious glomerulonephritis by Poststreptococcal and IgA nephropathy
61
what is most common in children and usually follows streptococcal pharyngitis? (1-4 weeks)
acute post infectious glomerulonephritis
62
what affects children and young adults resulting in hematuria 1-2 days post URT infection?
IgA nephropathy
63
when renal disease is associated with IgA nephropathy what happens? whats a hallmark of this disorder?
Hallmark: Henoch Schonlein Purpura | IgA nephropathy results in purpuric skin rash, GI pain, arthritis
64
What is a clinical syndrome, not a specific form of glomerulonephritis that is a progressive loss of renal functions that results in death from renal failure in weeks to months untreated
Rapidly Progressive Glomerulonephritis
65
What is a characteristic finding of Rapidly progressive glomerulonephritis
Crescentic glomerulonephritis due to proliferation of epithelial cells with infiltration of histiocytes
66
What happens when untreated glomerular disease leads to loss of glomeruli and tubules with fibrosis leading to the original renal disease not being able to be identified
chronic end stage renal disease
67
how can chronic end stage renal disease be detected? what is necessary for pt survival?
proteinuria, hypertension or azotemia at a routine exam | renal dialysis and kidney transplant are necessary for pt survival
68
what is the suppurative inflammation of kidney and renal pelvis caused by a bacterial infection called? what does it involve
acute pyelonephritis involves tubules, interstitial, and renal pelvis
69
how does a acute pyelonephritis infection spread? what cell is most prominent in the tubules of this disease
acute pyelonephritis infection spreads from bladder (Most commonly UTI) to the kidney through the blood neutrophils infiltrate the tubules (neutrophil casts)
70
what are the predisposing conditions to acute pyelonephritis?
UT obstruction, instrumentation, ureteral reflux, pregnancy, female gender, immunosupression, diabetes
71
what drugs may cause drug induced interstitial nephritis
ABs, NSAIDS, diuretics
72
What is the clinical aspect of drug induced interstitial nephritis? what cell is common from this disorder? what is missing from this disorder?
rapid onset (2-40 days) of fever, eosinophilia, renal dysfunction w hematuria, but little to no proteinuria
73
how do you treat drug induced interstitial nephritis? what is the prognosis and recovery time?
withdrawal of offending drug and with corticosteroids | prognosis is good w recovery in 6-8 weeks
74
what disorder has interstitial mononuclear cell infiltration and edema w many eosinophils, w non necrotizing granulomas
drug induced interstitial nephritis
75
what is a condition where renal function declines rapidly w evidence of tubular epithelial damage/ necrosis causing DEC GFR, oliguria, and electrolyte abnormalities
Acute Tubular necrosis
76
what are the causes of acute tubular necrosis? | Path findings of acute tubular necrosis?
acute tubular necrosis is caused by severe trauma, ischemia, septicemia, toxins path findings: dilation of tubules. edema. necrosis of tubular epithelium
77
Treatment of acute tubular necrosis? | Prognosis?
Tx of acute tubular necrosis is supportive care and dialysis | prognosis: in absence of preexisting conditions good
78
what is the thickening and sclerosis of renal arteries associated with benign hypertension called?
Arterionephrosclerosis
79
what is the genetics of Arterionephrosclerosis
Apolilipoprotein L1 gene, | Affects african americans same linkages as in FSGS
80
what is the pathology of Arterionephrosclerosis
small kidneys granular surface, hyaline arteriosclerosis. fibroelastic hyperplasia, tubular atrophy, global sclerosis of glomeruli
81
What may Arterionephrosclerosis also be seen with? this can lead to what symptoms?
Arterionephrosclerosis can be seen w Malignant hypertension also! causes INC cranial pressure (headache, nausea, visual impairment), proteinuria, ischemia leading to acute kidney injury
82
What is the pathology of Arterionnephrosclerosis caused by malignant hypertension
Hyperplastic arteriolosclerosis
83
whats an acquired defect in metalloproteinases that degrades vWD or an inherited ADAMTS 13 deficit?
thrombotic thrombocytopenia purpura (TTP)
84
what is caused by an endothelial cell injury from Shiga Toxin E coli, and is a major cause of acute kidney injury in children?
Hemolytic Uremic Syndrome (HUS)
85
What are TTP and HUS both related to?
TTP and HUS both lead to activation, aggregation, and consumption of platelets
86
Whats the pathology of TTP and HUS? specific site for TTP? specific site for HUS?
TTP/ HUS = widespread microthrombi in capillaries w RBC damage (schistocytes) TTP: primarily in kidney HUS: more widespread organ including CNS involvement
87
what clinical signs can urolithiasis (kidney stones) cause? | kinds of kidney stones?
maybe asymptomatic, obstruction, intense pain, infection, hematuria Calcium, Magnesium ammonium phosphate (staph infection), or uric acid (gout)
88
what is the dilation of renal pelvis/ calyces with parenchymal atrophy secondary to obstruction called
hydronephrosis
89
risk factors for hydronephrosis
renal stones, congenital UT obstruction, enlarged prostate, neoplasms, neurogenic bladder, pregnancy
90
what is a tumor that often invades renal vein commonly with pale clear cells.
Renal cell carcinoma Aka clear cell carcinoma
91
Risk factors for renal cell carcinoma?
male, smoking, hypertension, obesity, acquired polycystic disease due to chronic dialysis
92
clinical aspects of renal cell carcinoma
hematuria, mass, pain, fever, polycythemia (tumor producing EPO)
93
TX of renal cell carcinoma? | prognosis based on what
surgery and radiation, | prognosis is stage dependent
94
what is a common cancer in children that presents with an abdominal mass, pain, INC freq in some syndromes
Wilms Tumor
95
What does Wilms Tumor present with pathologically? | TX? prognosis?
triphasic proliferation of cells, with epithelial, stromal and blasternal components TX: surgery and chemo Prognosis: very good

Pathology Sp 16 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions