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Pathophysiology > unit 7 > Flashcards

unit 7 Flashcards

1
Q

Disorders of the Oral Cavity: Congenital Abnormalities

A

Cleft lip and Cleft Palate:

  • Arise in 6th to 7th week of gestation
  • Most likely of multifactorial origin
  • Feeding problems of the infant: high risk of aspirating fluid into respiratory passages
  • Speech development impaired
  • Surgical repair done as soon as possible
  • Therapy with speech-language pathologist and orthodontist
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2
Q

Disorders of the Oral Cavity: Inflammatory Lesions

A

Aphthous Ulcers:

  • Streptococcus sangius may be involved: part of the oral resident flora
  • Small painful lesions on movable mucosa, buccal mucosa, FOM, soft palate and lateral borders of the tongue
  • Usually heal spontaneousy
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3
Q

Disorders of the Oral Cavity: Infections *Thrush

A

Candidiasis:

  • Candida albicans is a causative agent that is often part of the resident flora and opportunistic organism
  • Oral candidiasis (thrush): people receiving broad-spectrum antibiotics, during and after cancer therapy and immunocompromised individuals or those with diabetes
  • May appear as a red, swollen areas
  • May be irregular patches of white curdle material
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4
Q

Disorders of the Oral Cavity: Infections *Herpes

A

Herpes Simplex Type 1 Infection:

  • Herpes simplex virus type 1 (HSV-1)
  • Transmitted by kissing or close contact
  • Virus remains dormant in sensory ganglion
  • Activated by stress, trauma, other infection, may result in the formation of blister, ulcers, clear fluid release- contains virus; can be autinoculated to other area. lesions heal spontaneously in 7 to 10 days
  • Acute stage may be alleviated by antiviral medication
  • May spread to eyes: conjunctives and keratitis
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5
Q

Disorders of the Oral Cavity: Infections *Syphilis

A
  • Caused by Treponema palladium
  • May cause oral lesions
  • Highly contagious during first and second stages
  • Primary stage: chancre, a painless ulcer on tongue, lip, palate, heals spontaneously (1 or 2 weeks)
  • Both stages treated with long acting penicillin
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6
Q

Disorders of the Oral Cavity: Dental Problems *Caries

A

Caries:

  • Streptococcus mutans: initiating microbe
  • Lactobacillus follows in large
  • Bacteria break down sugars and fermentable carbohydrates that produce large quantities of lactic acid and lower pH level in the mouth
  • Lactic acid dissolves mineral in tooth enamel
  • Tooth erosion and caries formation
  • Caries is promoted by frequent intake of sugars and acids
  • Fluoride: anticaries treatment
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7
Q

Disorders of the Oral Cavity: Dental Problems *Gingivitis

A

Gingivitis:

  • Changes in the gingiva may be a local or systemic problem
  • Inflammation of the gingiva: tissue becomes red, soft, swollen, bleeds easily and may be a result of accumulated plaque
  • Inadequate oral hygiene
  • Toothbrush trauma: results from improper or excessive brushing, that creates extensive grooving on tooth surface, which can increase plaque retention and damage to the gingiva
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8
Q

Disorders of the Oral Cavity: Dental Problems *Periodontitis

A

Periodontitis:

  • Infection and damage to the PDL and been
  • Predisposing condition is gingivitis
  • Caused by mircoorganisms as a result of poor self-care
  • Subsequent loss of teeth possible
  • Several categories, depending on degree of dx
  • May be aggravated by systemic diseases and medications that reduce salivary secretions
  • Periodontitis occurs when organisms enter the gingival bv’s and travel to the CT and bone of the dental arch
  • Resorption of bone and loss of ligament fibres results in weakened attachment of teeth
  • May result in total loss of tooth from socket
  • Treated by antimicrobials (ex: chlorohexdine), local surgery of gingiva and improved self-care
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9
Q

Disorders of the Oral Cavity: Dental Problems *Hyperkeratosis

A

Hyperkeratosis:

  • ex: Leukoplakia
  • Whitish plaque or epidermal thickening of mucosa
  • Occurs on buccal mucosa, palate, lower lip
  • May be related to smoking or chronic irritation
  • Lesions require monitoring: epithelial disposals beneath plaque may develop into squamous cell carcinoma
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10
Q

Disorders of the Oral Cavity: Cancer of the Oral Cavity

A
  • Squamous cell carcinoma (common type)
  • Often develops in persons older than 40 yrs: increase susceptibility to smokers, preexisting leukoplakia, alcohol abuse. Located on the FOM and lateral borders of the tongue and multiples lesions are possible
  • Kaposi sarcoma in patients with AIDS
  • Lip cancer has a better prognosis: common in smokers, particularly pipe smokers
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11
Q

Disorders of the Oral Cavity: Salivary Gland Disorders

A

Sialadenitis:

  • Inflammation of salivary glands
  • May be infectious or noninfectious
  • most commonly affects: parotid gland

Mumps: infectious parotitis

  • viral infection
  • Vaccine available

Noninfectious Parotitis:
-Often seen in older adults who lack adequate fluid intake and mouth care

Most malignant tumour of salivary glands is mucoepidermoid carcinoma

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12
Q

Describe Dysphagia

A

Difficulty swallowing

These cause dysphagia: neurological deficit, muscular disorders and mechanical obstruction

Results and presents as pain with swallowing, inability to swallow larger pieces of solid material and difficult swallowing liquids

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13
Q

Dysphasia Cont’: Neurological Deficits, Muscular Disorders and Mechanical Obstruction

A

Neurological Deficit:

  • Infection
  • Stoke
  • Brain damage
  • Achalasia: failure of the lower esophageal sphincter to relax because of lack of intervention

Muscular Disorders
-impairments fro muscular dystrophy

Mechanical Obstruction:

  • Congenital Atresia (atresia = death of cells) causes developmental anomaly and upper and lower esophageal segments are separated
  • Stenosis is narrowing of the esophagus, it may be developmental or acquired. May be secondary to fibrosis, chronic inflammation, ulceration, radiation therapy. It may also result from scar tissue. Stenosis requires treatment with repeated mechanical dilation
  • Esophageal Diverticula is an outputting of the esophageal wall and can be congenital or acquired following inflammation. It results in irritation, inflammation and scar tissue. Signs include dysphagia, foul breath, chronic cough and hoarseness
  • Tumors may be internal or external
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14
Q

Describe Esophageal Cancer

A
  • Primarily squamous cell carcinoma
  • Usually in distal esophagus
  • Significant dysphagia in later stages
  • Poor prognosis because of late manifestations
  • Associated with chronic irrigation because of chronic esophagitis, achalasia, hiatal hernia, alcohol abuse and smoking
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15
Q

Describe Hiatal Hernia

A

-Part of the stomach protrudes into thoracic cavity
Types:
-Sliding hernia is a more common type. It is portions of the stomach and gastroesophageal junction slide above the diaphragm
-Rolling/paraesophageal hernia is part of the funds of the stomach that moves up through an enlarged or weak hiatus in the diaphragm and may bemuse more trapped

-Food may lodge in such of hernia and cause inflammation of the mucosa, reflux of food up the esophagus and can lead to chronic esophagitis

Signs:

  • Heartburn or pyrosis
  • Frequent belching
  • Increased discomfort when laying down
  • Substernal pain that may radiate to shoulder and jaw
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16
Q

Describe Gastroesophageal Reflux Dx

A
  • Periodic reflux of gastric contents into distal esophagus causes erosion and inflammation
  • Often seen in conjunction with hiatal hernia
  • Severity depends on compentance of lower esophageal sphincter
  • Delayed gastric emptying maybe a factor
  • Avoid caffeine, fatty and spicy foods, alcohol, smoking and certain drugs
  • Use of medication may reduce reflux and inflammation
17
Q

Hepatitis

A
  • Inflammation of the liver
  • Liver has over 200 functions, so inflammation can be very serious
  • Many factors can cause liver dx
  • Focus on viral hepatitis. 5 virus are currently known to affect liver directly and other virus affect liver secondarily
  • Cell damage in hepatitis leads to inflammation and necrosis: severe damage –> binary stasis –> cholmeia (bile in blood)
  • biliary stasis (not moving), bile is not moving
18
Q

Viral Hepatits

A

Liver damage in viral hepatits occurs by distinct mechanisms:

  • Intercellular virus replication results in hepatocyte (liver cells) lysis (bursting opening) causing cytopathic effect (CPE: directly killing other cells around it) ex: HCV infection
  • Agressive immune response to virally infected cells causes severe inflammation and hepatocyte damage ex: HBV infection
  • The diseases caused by hepatitis virus range in severity: subclinical (unaware of infection), ruminant hepatitis (symptoms of hep) and liver failure
  • Possible outcomes of infection are variable and may result in regeneration of tissue, scar tissue formation = no regeneration (fibrosis and cirrhosis) and heptocellular carcinoma
  • Liver function is highly dependent upon liver architerture
  • Scarring from cirrhosis affects liver architecture and prevents bile flow (biliary stasis) and prevents normal blood flow (ischemia)
19
Q

Acute vs Chronic Hep

A
  • HAV and HBV usually run an acute course
  • Viral antigens provide window on course of disease
  • In some cases, individual is unable to resolve infection and it becomes chronic, leads to fibrosis, cirrhosis and hepatocellualr carcinoma. Occurs in 5-10% of cases of adult onset HBV infection and occurs in great than 50% of cases of HCV infection
  • HBV infection may be transmitted from mother to neonate which results in high incidence of chronic carriers and there carriers may be asymptomatic for many years (though still highly infectious)
20
Q

Etiology of Hep

A

*RNA virus uses RNA to replicate there viruses

Hep A Virus (RNA virus)

  • Transmitted usually by fecal-oral route
  • Effective vaccine available

Hep D Virus (RNA virus)

  • Cannot replicate on its own, so it requires and HVB co-infection
  • Blood borne transmission (high rate in IV drug users)

Hep E Virus (RNA virus)
-Similar to HAV, but may cause more serious infection (especially in Asia and Africa)

21
Q

Etiology Cont’ Hep C Virus Infection

A
  • Single stranded RNA virus that mutates frequently (like HIV) and the virus changes antigens too frequently to make a vaccine possible
  • Tranmission is percutaneous exposure to blood products such as, intravenous drug use, hemodialysis and blood transfusion. It can also be transmitted through high-risk sexual behaviour
  • About 70% of HCV infections fail to resolve and lead to chronic infection: estimate 170 million (3%) of world population chronically infected
  • Chronic infection sequelae such as, cirrhosis (10-20%) *refer to ppt and hepatocellular carcinoma (HCC) frequency 20x higher in Chronic HCV/cirrhosis patients
22
Q

Etiology Cont’ Hep B Virus Infection

A
  • US estimate: 200,000 - 250,000 cases/year
  • 4000-5000 US deaths/years from chronic infections sequelae
  • Global estimate 300 - 400 million active infections, largely in Asia and Africa
  • Modes of HBC transmission are direct: blood to blood (IV drug use), sexual transmission and mother to neonate
  • HBV is a DNA virus: stable expression of HBV antigens
  • Effective vaccine is available: often combined with vaccine for HAV

Chronic Hep B Infection:

  • Risk of infection caries inversely with age: 90% of neonatal or perinatal infections become chronic, 20-25% 0f infections in 1-5 yrs old children become chronic
  • people often don’t know they are affected (carriers), which causes them to pass it along more frequently
  • Explanation for frequency pattern lies in how the immune response words
  • Neonates have immautre immune systems that are still learning to distinguish self for non self
  • Neonate sees virus-infected cells as normal tissue and learns to recognize self (immunological tolerance)
  • No immune aggression against virus therefore, later in life, tolerance breaks down (not enough cure) and immune response cause hepatocyte damage and symptoms of infection
23
Q

Chronic HBV vs Chronic HCV

A
  • Chronic HBV infection results because of a failure of immune system to response
  • Chronic HCV infection results in spite of otherwise well activated immune response
24
Q

Hepatits: Signs and Symptoms

A

3 stages recognized in course of infection:
Pre-icteric stage (no jaundice)
-prodromal phase (signs there was something wrong, bot no other signs, so when you look back you recognize somethings was wrong)
-S/S vague, ill-defined

Icteric stage (jaundice) 
-S/S reflect impaired function of inflamed/damaged liver causing
swelling (hepatomegaly) and pain, elevated clotting time (blood is not clotting fast enough due to decrease in clotting factors that the liver can not produce), decrease clotting factors = jaundice --> decreases bilirubin metabolism = light coloured stools and dark urine

Post-iceric stage (recovery, however, this may not always happen and chronic hep can occur)
-resolution of infection ameliorates signs and symtpoms

Signs and symptoms are a reflection of the stage

25
Q

Treatment of Hep

A

Immunomodulators: interferon alpha may stimulate immunity to virus

Antiviral agents reduce HBV virtual burden:
-Entecavier (baraclude: good against the one that are otherwise resistant

26
Q

Describe Cirrhosis

A
  • Progressive liver destruction resulting form a number of liver dx
  • After 80-90% of liver damaged –> liver failure
  • 50% of cases are related to alcohol consumption
  • Categorized based upon cause alcoholic liver dx (50% of cases), biliary cirrhosis (immune disorders or cholestasis), post-nectroic cirrhosis (hep or chemical exposure) and metabolic (iron storage disorders)
27
Q

Cirrhosis- Pathophysiology

A

Insult leads to fibrosis in normal liver architecture:

  • Distortion of lobule bile ducts and blood vessels impairs function
  • Ischemia, biliary backup –> inflammation, more damage

Initially see swelling (edema) of the whole architecture

Later see shrinkage as fibrosis progresses

Pathophysiology is related to:

  • loss of normal hepatocyte function
  • Damage to liver architecture affecting bile flow
  • Damage to liver architecture affecting blood flow
28
Q

Cirrhosis Pathophysiology Loss of Function

A

Issues related to loss of normal hepatocyte function:

  • Impaired bilirubin metabolism –> jaundice
  • Impaired bile production –> impaired nutrient absorption
  • Impaired clotting factor production –> bleeding
  • Impaired albumin production (the major protein of the plasma in blood that is made by the liver) –> edema
  • Decreased iron/vitamin B12 storage –> anemia
  • Impaired steroid inactivation (if the liver cant get rid of this hormone) –> gynecomastia (breast development in men)/oligomenorrhea
  • Impaired detoxification –> neurologic symptoms of ammonia build up (ex: encephalopathy)

Perfect exam question:
ex: Cirrhosis affect the normal function of hepatocytes which causes impairments of the bilirubin metabolism causing an end result of jaundice

29
Q

Cirrhosis Pathophysiology: Impaired Bile Flow

A

Issues related to damage to liver architecture that impairs normal liver bile flow:

  • Obstructive jaundice (backup of bile in over)
  • Malnutrition (reduced bile in intestine)

Issues related to damage to liver architecture impairs normal liver blood flow

Hepatic portal system hypertension:
–> splenomegaly (hemolytic jaundice and decrease platelets (clotting factors, won’t clot blood)) –> malnutrition (congestion in stomach and intestines) –> Esophageal varices (varicose veins) –> ascites (fluid accumulation in abdomen, 2 spaces of fluid, intersittial spaces and plasma in blood, hydrostatic pressure pushes fluid out and osmotic pressure pushes fluid into the blood, therefore to much push and less pull leads to ascites)

30
Q

Signs, Symptoms and Complications of Cirrhosis

A

Vague and indeterminate in initial stages

Later reflect liver damage, bile/blood flow issues such as,

  • Peripheral edema
  • Ascites
  • Bruising (low clotting factors, from low platelets)
  • Jaundice
  • Sexual Effects: gynecomastia, impotence, testicular atrohpy and oligomenorrhea
  • Encephalopathy
31
Q

Cirrhosis Treatment

A

Cannot cure, so options are limited:
Transplantation (especially partial liver transplant)

Supportive Therapies based upon s/s:

  • Peripheral edema –> albumin infusion
  • Ascites –> paracentesis and albumin infusion
  • Bruising –> clotting factor replacement
  • Jaundice –> ?
  • Sexual effects –> hormone inhibitors
  • Encephalopathy –> antibiotics to reduce ammonia made by intestinal flora

Pathophysiology (9 decks)

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