PT hepatic issues Flashcards
1
Q
What is the function of the liver
A
- production of bile to help carry away waste products
- regulation of glucose, hormones, and vitamines
- metabolizes drugs, alcohol and chemicals
- production of proteins for blood plasma and regulation of blood clotting
2
Q
What are common physical signs of liver disease
A
- hepatomegaly
- spider angiomas/nevi
- Jaundice
- ascites
- gynecomastia
- carpal tunnel syndrome (back up of fluid)
3
Q
A
4
Q
review pathology
A
5
Q
What is hepatic encephalopathy
A
- poor liver function leads to accumulation of ammonia
- ammonia is a neurotoxin
- damages astocytes
- can lead to cerebal edema, inceased in intacranial perssure
- assoicated with increased incidence of intarcerebral hemorrhage
- severity graded by 0-4
- minimal cognitive changes to coma
6
Q
What are some causes of hepatic encephalopathy
A
- renal failure/dysfunction
- GI bleeding
- infection
- constipation (contibutes to another dysfunction)
- medications
- diuertics
7
Q
What are some causes of liver disease/dysfunction
A
- hepatitis
- drug induced injury/hepatotoxicity
- alcoholic liver disease
- non-alcoholic fatty liver disease
- autoimmune disease (autoimmune hepatitis can affect bile ducts)
- pregnancy induced
- vascular
- neoplasm
- pyogenic liver abscess
8
Q
Describe the types of hepatitis
how are they transmitted/is there a vaccine
A
- HAV: transmission though oral-fecal and there is a vaccine
- HBV: trasmission through sex, skin puncture, with a vaccine
- HCV: transmission though injection drug use; no vaccine
- HDV: transmission with co-infection with HBV; HBV vaccine
9
Q
common signs and prognosis for hepatitis
A
- jaudice, fever
- prognosis varies from recovery to chronic liver disease
10
Q
How to address non-alcoholic fatty liver disease
A
- goal to prevent long-term liver damage and sequelae: reduce liver fat
- overall weight loss 3-10% of body weight may help
- weight loss needs to occur with health diet changes
- long-term damage can lead to end stage liver disease
- lifestyle interventions
- dietary resriction: processed foods, sugarry foods, complex carbs
- increased physical activity
11
Q
What is hepatopulmonary syndrome
A
- defect in arterial oxygenation caused by intrapulmonary vascular dilations in the context of liver disease
- prevalence in patients who are candidates for liver transplant (4-32%)
- diagnosed with arterial blood gas and transthroacic echocardiogaphy
- liver disease caused inflammatory response in lungs
12
Q
Mechanism of hepatopulmonary syndrome
A
- endotoxemia: liver isnt clearing toxins well
- causes movement of intestinal bacteria into body
- increase of macrophages and monocytes in lungs
- results in increase TNF and NO (inflammation/vasodilation)
overall: ventilation-pefusion mismatch, mos significant in base of lungs
13
Q
How can hepatopulmonary syndrome by staged
A
- Mild: PaO2= ≥80 mmHg
- moderate = PaO2 60-79 mmHg
- Severe = PaO2 50-59 mmHg
- Very sever = PaO2 < 50 mmHg
important factor related to time to transplant and prognosis
14
Q
Clinical manifestations of hepatopulmonary syndrome
A
- dyspnea: at rest or exertion
- platypnea orthodeoxia: worsening symptoms in upright positioning
- digitla clubbing
- normal chest radiographs
- rarely: cyanosis
15
Q
how does HPS differ from common lung disease
A
- driven by liver disease
- preservation of lung tissue
- no changes on imaging
- platypnea orthodoeoxia
16
Q
what is the medical treatment for HPS
A
- supplemental oxygen for symptom management
- liver transplant
- transplant only effective long term teatment
- will no qualify for transplant if too severe (< 40 mmHG)
17
Q
outcomes fo medical treament/transplantation for HPS
A
- longer mechanical ventilation time, an increase need for non-invasive ventilation, longer intensive care unit stay and longer hospital stay
- five year survival rate 76%
- resolution of gas exchange abnormalities can occur in 6 to 12 months abnormalities can persist after 12 months
- mortality with or without transplant is highest in patients with PaO2 < 50 mmHg
18
Q
Premature infants, fractures and nutrition
A
- premature infants are among those at highest risk for hospital acquired fractures
- about 1/3 of ELBW neonates sustained fracutres
- nutritional prevention and treatment important
- attempting to mimic in utero nutrition
- TPN: may help increase intake of nutrients and minerals improving growth and lowering risk of fractur
19
Q
nutritional considerations for geriatric population
A
- changes in nutrition requirements
- changes in lean body mass
- sacropenia/osteosacropenia
- physical impairments: dentition
- comorbidities
- psychosocial and cognitive changes
20
Q
nutritional screening and PT
A
- screen for overweight and obesity
- BMI, waist circumference, risk factors for disease assoicated with obseity
- screen for under nutrition: mini nutritional assessment tool
- dietary changes/refferrals to dietitians
21
Q
PT exam with nutrition
A
- appearance nad postural analysis
- motor and sensory function
- functional activities
- gait, endurance, and postural control
- egress test
22
Q
RA and nutrition
A
- anti-inflammatory diet may be helpful for RA and other conditions with chronic inflammation
- omega -3 fatty acids
- capsaicin
- ginseng
- cocoa
- Vit D
23
Q
What is important parts of an anti-inflammatory diet: fruits/veggies
A
- 3-4x more veggies than fruit
- 1-2 servings/color/day variety
- antioxidants neutralize oxidative stress
- minerals, vitamins, fibers, polyphenols
- intake inversely coorrrelated with obesity and inflammation
- legumes and beans
24
Q
whole grains: anti-inflammatory diet
A
- affects microbiome and immune function via Short chain fatty acid production
- reduces oxidative stess and inflammation
- grain with 1 ingredient only
25
Q
foods that promote inflammation
A
- processed foods
- refined starches and grains
- sugar
