Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PC-705 > Module 4 > Flashcards

Module 4 Flashcards

GI, Liver, Biliary, Neuro (84 cards)

Start Studying
1
Q

Primary cause of GERD

A

Backup of chyme (acid, pepsin) into the esophagus

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

Causes of esophagitis

A

GERD, infections, medications (NSAIDS), allergies

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

Cell changes in Barrett’s esophagus

A

Squamous cell epithelial -> metaplastic columnar; is a precursor to adenocarcinoma

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

Risk factors for esophageal cancer

A

Males, > 60 years old, smoking/alcohol, dietary, East Asia/Africa

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

Types of esophageal cancer

A

Squamous Cell: in upper/middle esophagus, associated with tobacco/alcohol
Adenocarcinoma: lower esophagus, associated with GERD and Barrett’s esophagus

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

Cause of peptic ulcer disease

A

Stomach/duodenal lesions in the muscularis musocae, caused by NSAID and H pylori

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

How do NSAIDs cause mucosal injury in gastritis?

A

They block COX enzyme (produces prostaglandins - protect the stomach lining by stimulating mucus and bicarb production); they increase gastric acid secretion

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

How does autoimmune gastritis affect the hematological system?

A

Autoantibodies attack the parietal cells (help with nutrient absorption)
-Vitamin B12 and Fe deficiency

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

Major risk factor for developing intestinal gastric cancer

A

Environmental factors (H PYLORI, smoking/alcohol, toxins

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

Major risk factor for developing diffuse gastric cancer

A

Genetic mutations (family hx, hereditary diffuse gastric cancer [HDGC], pernicious anemia

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

Gastric subtype associated with H pylori

A

Involved in both acute and chronic, but chronic is only type B (from environmental factors)

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

Patho of Crohns

A

Autoimmune: The immune system attacks the GI tract, leading to chronic inflammation. Triggers macrophages and dendritic cells involves T-helper cells (Th1 and Th17), and releases pro-inflammatory cytokines (TNF-α). Has periods of flare-ups and remission.

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

Intestinal strutcure of Crohns

A

Transmural Inflammation: patchy areas on inflammation which affects all layers of the tissue. COBBLESTONE appearance (GRANULOMAS), SKIP LESIONS, and ulcers.

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

Where is Crohns located?

A

Any part of GI tract

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

Lab results for Crohns

A

↑ CRP and ESR. CBC often shows anemia, leukocytosis, and thrombocytosis

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

Patho of UC

A

Risk factors (genetics, environmental, immune response, and DYSBIOSIS) leads to inflamed colonic mucosa.
Innate: macrophages engulf pathogens and release pro-inflammatory cytokines (TNF-α, IL-1β) and neutrophils form CRYPT ABCESSES
Adaptive: Th2 dominated response release IL-5 and IL-13, and T-reg cells are impaired which leads to inflammation.

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

Intestinal Structure of UC

A

Mucosal and submucosal inflammation, starts in rectum and extends proximally. Has continuous inflammation and bloody stool is common.

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

Location of UC

A

Limited to colon and rectum

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

Lab results for UC

A

↑ CRP and ESR. CBC often shows anemia, leukocytosis, and thrombocytosis.
↑ fecal calprotectin and lactoferin
p-ANCA antibody + in UC

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

Patho of IBS

A

Gut-brain axis dysregulation; increased cortisol levels and CRH receptor expression in GI tract are observed in IBS

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

Acute Pancreatitis

A

Premature activation of pancreatic enzymes which leads to autodigestion and pancreatic tissues. This activates trypsin, and local inflammation leads to SIRS.

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

Risk factors for acute pancreatitis

A

GALLSTONES, alcohol, hyperlipidemia, hypercalcemia, and medications

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

Chronic Pancreatitis

A

Progressive inflammatory condition with irreversible structural damage which leads to fibrosis, is associated with recurrent episodes of acute pancreatitis and ongoing injury.

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

Risk factors for pancreatic cancer

A

Chronic pancreatitis, smoking, obesity, family hx, genetics (KRAS), and long-term diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Patho and transmission of Hep A
Acute; fecal-oral
26
Diagnostic Tests for Hep A
+ HAV IgM
27
Patho and Transmission of Hep B
Acute and chronic, chronic leads to cirrhosis/liver cancer; blood, sexual, perinatal
28
Diagnostic Tests for Hep B
+ HBsAg + IgM & Anti-HBs + HBV DNA
29
Patho and Transmission of Hep C
Asymptomatic when early, can develop chronic and develop cirrhosis/liver cancer; blood, IV drug use
30
Diagnostic Tests of Hep C
+ Anti-HCV antibodies + IgG & HCV RNA
31
Patho and transmission of Hep D
Chronic infection and worsens HBV, increases liver disease and cirrhosis; requires co-infection with HBV replicate; blood
32
Diagnostic Tests of Hep D
+ Anti-HDV antibodies + IgG & HDV RNA
33
Patho and transmission of Hep E
acute infection; fecal-oral (contaminated water)
34
Diagnostic Tests for Hep E
+ HEV IgM + HEV RNA
35
Which immunoglobulin is associated with recent/active infection?
IgM
36
Which immunoglobulin is associated with past infection/immunity?
IgG
37
Patho of cirrhosis
repeated injury to liver triggers fibrosis/scarring
38
Stage 1 of Cirrhosis
Fatty liver (steatosis), is reversible with lifestyle changes
39
Stage 2 of Cirrhosis
Inflammation fibrosis, start of permanent damage
40
Stage 3 of Cirrhosis
advanced fibrosis with regenerative NODULES, significant liver impairment
41
Stage 4 of Cirrhosis
ESLD, severe scarring and liver failure
42
Complications Associated with Cirrhosis: Portal HTN
↑ pressure in portal vein from scarring, blood is redirected into other vessels and forces fluid into peritoneal cavity
43
Complications Associated with Cirrhosis: Hypoalbuminemia
↓ albumin leads to reduced oncotic pressure where fluid can leak and cause third-spacing
44
Complications Associated with Cirrhosis: Splanchnic Vasodilation
dysfunctional liver triggers release of vasodilatory substances, causing increased blood flow to portal circulation worsening portal HTN
45
Complications Associated with Cirrhosis: ↑ lymph production and leakage
portal HTN increases exess lymph production, the damaged liver cannot drain excess fluid and leaks into peritoneal cavity and causes ascites
46
Complications Associated with Cirrhosis: Activation of RAAS
from relative hypovolemia caused by splanchnic vasodilation, causes Na and H2O retention further worsening ascites
47
Complications Associated with Cirrhosis: Systemic Inflammation
in advanced diseases; has a possibility of ↑ inflammatory mediators and bacteria and leaks to more leakage of fluid in the abdomen
48
Complications Associated with Cirrhosis: Hepatic Encephalopathy
toxins (AMMONIA, urea) accumulate and impair brain fxn
49
Complications Associated with Cirrhosis: esophageal and gastric varices formation
↑ portal pressure causes collateral circulation backup into venous system
50
Lab findings associated with cirrhosis
↑ AST, ALT, ALP, GGT, Bilirubin ↑ PT/INR time (reduced production of clotting factors) ↓ albumin, platelets, Na
51
Patho of MASLD
Accumulation of fats (steatosis) exceeding 5% of liver cells WITHOUT ALCOHOL CONSUMPTION.
52
Complications of MASLD
Insulin resistance, lipotoxicity, oxidative stress (ROS production damages mitochondria), and inflammation (Kupffer cells release cytokines like TNF-α, IL-6, and IL-1β), genetic susceptibility
53
Patho of MASH
Worsened form of MASLD, liver shows both steatosis and inflammation along with liver injury
54
Complications of MASH
Cell death (apoptosis and necrosis release DAMPS) BALLOONING DEGENERATION (hepatocytes lose normal shape, become swollen and round) MALLORY-DENK BODIES (shows ongoing inflammation) Fibrosis Initiation (stellate cells produce collagen, replacing healthy liver tissue with scar tissue)
55
Risk Factors for MASLD / MASH
Obesity, T2DM, metabolic syndrome, sedentary lifestyle, poor diet, genetics DYSBIOSIS: imbalanced gut microbiome which affects bile acid metabolism and promotes inflammation
56
Dopamine: roles and disorders
Excitatory and inhibitory; inhibits unnecessary movements and release of prolactin, stimulates the secretion of growth hormone. DEC LEVEL: Parkinson's addiction INC LEVEL: ticks, Schizophrenia
57
Serotonin: roles and disorders
Excitatory/INHIBITORY; regulates temp, perception of pain, emotions, and sleep cycle DEC LEVEL: anx/dep, insomnia
58
Norepinephrine: roles
Excitatory; increases alertness and wakefulness, stimulates various processes of the body
59
Acetylcholine: roles
Excitatory except in heart; regulates sleep cycle, essential for muscle function
60
GABA: roles
Inhibitory; reduces neuronal excitability throughout nervous system
61
Causes of bacterial meningitis in adults
STREPTOCOCCUS PNEUMONIAE; Neissseria meningitis
62
Causes of viral meningitis in adults
Enteroviruses (Coxsackie, echoviruses), arboviruses (west nile, zika), mumps, HSV, varicella
63
Causes of bacterial meningitis in neonates
GBS, E coli, listeria
64
Causes of bacterial meningitis in older children
Streptococcus pneumoniae
65
Causes of viral meningitis in neonates
HSV-2
66
Causes of viral meningitis in older children
Varicella
67
Patho of viral meningitis
Virus enters through bloodstream or reactivation; generally milder with gradual onset but still significant
68
Patho of bacterial meningitis
Bacterial invasion occurs through bloodstream directly into CNS from infections, trauma, or sinusitis Severe and often life-threatening, rapid onset of symptoms with high morbidity and mortality rates
69
Patho of Guillian-Barre Syndrome
Autoimmune disease triggered by infections which cause nerve blocks
70
Clinical features of Guilian-Barre Syndrome
Rapid onset, symmetrical muscle weakness, ascending paralysis, decreased/absent reflexes Severe Cases: respiratory muscle involvement needing mechanical ventilation
71
Ischemic Stroke
Obstruction of bloodflow from thrombus/embolus, reversible if reperfusion occurs quickly
72
Causes of ischemic stroke
Atherosclerosis, HTN, DM, hyperlipidemia
73
Embolic Stroke
Type of ischemia stroke Clot or debris travels from another part of the body and lodges in brain artery
74
Causes of embolic stroke
A fib, carotid artery disease, endocarditis, valve disorders
75
Thrombotic Stroke
Type of ischemic stroke From blood clot that forms directly in artery which gradually narrows the artery
76
Causes of thrombotic stroke
Athersclerosis leading to stenosis, or hypercoagulable states
77
Patho of multiple sclerosis
Chronic autoimmune disease that affects CNS. Immune-mediated attack on CNS: T-cells attack myelin, B cells produce antibodies that target myeline. Cytokines (TNF-α, IFN-γ, and IL-17) are released causing further inflammation Demyelination: loss of myelin sheath slows/blocks nerve signal conduction, forms sclerotic plaques in white matter Axonal Damage: secondary from chronic inflammation and demyelination, causing progressive disability
78
Hallmark of ALS
Progressive degeneration of motor neurons in brain and spinal cord. Leads to muscle weakness, paralysis, and respiratory failure. Loss of neurons results in the inability to send signals to muscle causing atrophy
79
Hallmark of Myasthenia Gravis
Autoimmune destruction of acetylcholine receptors or related proteins at neuromuscular junction. Antibodies block/destroy ACH receptors, preventing muscle contraction.
80
Primary mechanism of Bell's Palsy
Sudden, unilateral paralysis from dysfunction of cranial nerve VII (facial nerve). Linked to viral infection, but exact cause unknown.
81
Primary mechanism Trigeminal neuralgia
Chronic pain affecting trigeminal nerve (cranial nerve V). Involves vascular compression of trigeminal nerve root. Leads to demyelination of nerve fibers, leading to sudden and sharp facial pain.
82
Primary mechanism of migraines
Involves cortical spreading depression (neuronal depolarization then suppression which spreads across cerebral cortex). Leads to inflammatory and vascular changes. Releases vasoactive peptides (CGRP). Plays a key role in vasodilation, neurogenic inflammation, and pain sensation.
83
Trigger for migriane with aura
Cortical spreading disease. Aura symptoms include flashing lights, visual disturbances, tingling, numbness. Others include stress, hormonal fluctuations, dietary factors, changes in weather/barometric pressure
84
Primary mechanism of tension-type HA
Involve peri-cranial muscle tension and heightened pain pathway Do not involve CSD or activation of trigeminovascular system. Prolonged muscle contraction and stress leads to pain, can progress to chronic HAs but lacks severe neurological symptoms seen in migraines

PC-705 (3 decks)

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